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A major win for sportsmen and women arrives as critical access and conservation fights continue. The conservation landscape never stays quiet for long. This week's Sportsmen's Voice Roundup covers a major milestone for sportsmen and women nationwide as North Carolina Governor Josh Stein becomes the 29th member of the Governors Sportsmen's Caucus, strengthening bipartisan support for hunting, fishing, and outdoor recreation at the highest levels of state government. CSF's Conner Barker joins the show to explain why gubernatorial engagement matters and how direct relationships with governors can help advance pro-sportsmen legislation while stopping harmful policies before they become law. The conversation also explores several pressing issues facing North Carolina hunters, including ongoing efforts to modernize the state's Sunday hunting restrictions and improve access for sportsmen across diverse hunting opportunities ranging from coastal waterfowl hunting to black bear, deer, and turkey hunting. The episode also delivers updates from around the country. In New Hampshire, efforts to secure much-needed conservation funding through hunting and fishing license fee increases have been delayed. In Michigan, lawmakers are considering proposals that would expand commercial fishing practices for walleye, yellow perch, and lake trout, raising concerns among anglers and conservation advocates. Out west, California legislators continue debating several bills affecting bowhunters, firearm owners, and public land hunting access. Whether you're following wildlife conservation policy, public land access, hunting regulations, or fisheries management, this roundup provides a practical look at the decisions shaping the future of America's sporting traditions. Follow the show for more weekly hunting and fishing conversations shaping the future of the outdoors. Get the FREE Sportsmen's Voice e-publication in your inbox every Monday: www.congressionalsportsmen.org/newsletter Follow The Sportsmen's Voice wherever you get your podcasts: https://podfollow.com/1705085498 Learn more about your ad choices. Visit megaphone.fm/adchoices
Dr. Margarita Fedorova discusses the effectiveness of shunting for idiopathic normal pressure hydrocephalus. Show citation: Luciano MG, Williams MA, Hamilton MG, et al. A Randomized Trial of Shunting for Idiopathic Normal-Pressure Hydrocephalus. N Engl J Med. 2025;393(22):2198-2209. doi:10.1056/NEJMoa2503109 Show transcript: Dr. Margarita Fedorova: Welcome to Neurology Minute. My name is Margarita Fedorova and I'm a neurology resident at the Cleveland Clinic. Today we're reviewing a randomized trial that provides high quality evidence for treatment we've been using for decades, shunting for idiopathic normal pressure hydrocephalus. The PENS trial, a placebo controlled effectiveness and iNPH shunting trial was published in the New England Journal of Medicine in December 2025 by Luciano and colleagues. This international multicenter study enrolled 99 patients across the United States candidate in Sweden. While idiopathic normal pressure hydrocephalus or iNPH is characterized by triad of gait impairment, cognitive decline in urinary continence, these findings can be non-specific and we mass factor in radiological findings too. Furthermore, while CSF shunting has long been the standard treatment, its effectiveness has never been rigorously confirmed in a large well-powered randomized trial. In this trial, patients with a clinical improvement in gait velocity after temporary CSF drainage were deemed eligible for shunting and randomizing the trial. What makes this trial particularly elegant is its blending strategy. All 99 participants underwent the same surgical procedure with the same commercially available programmable shunt valve. After surgery, the valve was set either to an open functioning position or to a high resistance placebo setting. Neither patients nor assessors knew who had a working shunt. This is about as close to a true double-blind design as neurosurgery can get. The primary outcome was changing gait velocity at three months. The open shunt group improved by 0.23 meters per second on average, while the placebo group showed essentially no change in 0.03 meters per second. That's a treatment difference of 0.21 meters per second, both statistically significant and clinically meaningful. To put that in perspective, a change of 0.10 meters per second is considered the threshold for substantial meaningful change in the elderly. 80% of the open shunt group exceeded that threshold compared to only 24% of the placebo group. The Tenet scale, which measures gait imbalance, also showed significant improvement in the open shunt group. However, screening measures for good condition using the MoCA scale and bladder symptoms did not reach significance at three months, though tertiary outcomes for cognitive testing, quality of life and functional independence tended in favor of shunting. Importantly, falls were more common in the placebo group at 46% compared to 25% in the open shunt group. This is a meaningful safety signal given how dangerous falls are in older adults. There were also real risks with active shunting. Subdural hematomas occurred in 12% of the open shunt group versus 2% of placebo and three even required surgical intervention. Positional headaches from low CSF pressure were more common in the open shunt group at 59% versus 28%. The good news is that the adjustable valve allowed non-invasive management of many of these complications. While this trial gives us reasons to be cautiously optimistic about shunting for appropriately selected iNPH patients, it's worth noting that we only have evidence for improvement in gait and follow-up is only three months. Longer-term data is still being collected so we don't know yet how durable these benefits are. If you want to read more, please find the paper by Mark G. Luciano, et al. It's titled A Randomized Trial of Shunting for Idiopathic Normal Pressure Hydrocephalus published in the New England Journal of Medicine in December 2025. That's your neurology menu for today. Keep exploring and we'll see you next time.
In this episode of Head and Neck Innovations, Edward Doyle, MD, and Varun Kshettry, MD, join host Paul Bryson, MD, to discuss the diagnosis and management of cerebrospinal fluid (CSF) leaks and encephaloceles. They explore common presentations, advances in imaging and diagnostic testing, and collaborative surgical approaches for skull base repair. The conversation also highlights the growing recognition of idiopathic intracranial hypertension as an underlying cause of spontaneous CSF leaks, as well as emerging treatment strategies including venous sinus stenting, weight management, and GLP-1 receptor agonists.
Historic access wins and conservation funding advances are reshaping the future of America's hunting and fishing opportunities. The biggest hunting and fishing access expansion in U.S. history just landed, and the implications for sportsmen across the country are massive. This week's Sportsmen's Voice Roundup breaks down the Department of the Interior's proposal to expand more than 1,400 hunting and angling opportunities across National Wildlife Refuges in 32 states. Listeners get a ground-level look at what expanded public land access means for waterfowl hunting, turkey hunting, freshwater fishing, and long-term wildlife management. The conversation also digs into the reauthorization of the Sport Fish Restoration and Boating Trust Fund, one of the most important conservation funding mechanisms supporting fisheries conservation, boating infrastructure, and aquatic habitat restoration nationwide. If you care about the future of fishing, public access, and state-led fish and wildlife conservation, this segment explains why the highway bill matters far beyond Washington politics. Additional updates cover Alaska's legislative victories for hunters and guides, Louisiana's movement on sportsmen privacy protections, and New Hampshire's ongoing discussion surrounding hunting and fishing license fee increases. The episode closes with a preview of CSF's Hunt Fish 250 campaign celebrating America's outdoor heritage and the freedom to hunt and fish. Follow the show for more weekly hunting and fishing conversations shaping the future of the outdoors. Get the FREE Sportsmen's Voice e-publication in your inbox every Monday: www.congressionalsportsmen.org/newsletter Follow The Sportsmen's Voice wherever you get your podcasts: https://podfollow.com/1705085498 Learn more about your ad choices. Visit megaphone.fm/adchoices
Dans ce deuxième épisode d'On Jase Business avec Laura Saad, CSF et planificatrice financière, on plonge dans une discussion ultra authentique sur les finances personnelles, la discipline, la croissance entrepreneuriale et le développement personnel. On parle notamment de :
Advances in immunotherapies for multiple sclerosis and related disorders have increased the risk of infections and raised important questions about vaccination efficacy. This episode reviews infection risks across treatment classes, emphasizes the importance of monitoring and patient education, and discusses optimal vaccine timing to preserve protective immune responses. In this episode, Aaron L. Berkowitz, MD, PhD, FAAN, speaks with Avindra Nath, MBBS, FAAN, coauthor of the article "Infection Risk and Vaccine Considerations in Multiple Sclerosis and Related Disorders" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology in the Department of Neurology at the University of California, San Francisco, in San Francisco, California. Dr. Nath is the chief of the Section of Infections of the Nervous System at the National Institute of Neurological Disorders and Stroke, National Institutes of Health, in Bethesda, Maryland Additional Resources Read the article: Infection Risk and Vaccine Considerations in Multiple Sclerosis and Related Disorders Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Full episode transcript available here Dr Berkowitz: Over the last decades, there has been a revolution in the treatment of multiple sclerosis, neuromyelitis optica spectrum disorder, and other immune-mediated neurologic conditions with countless new, highly effective medications. However, with every new treatment comes new risks; and in the case of immunomodulatory therapy, many of those risks relate to infection. Today, I have the privilege of talking with an expert on this topic, Dr Avindra Nath, about the infectious risks of treatments for multiple sclerosis and other immune-mediated neurologic disorders. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Avi Nath about his article on vaccine considerations and infection risk in multiple sclerosis and related disorders, which he coauthored with Dr Amit Bar-Or. This article appears in the April 2026 Continuum issue on multiple sclerosis. Welcome to the podcast, Dr Nath, and could you please introduce yourself to our audience? Dr Nath: Thanks very much for inviting me to this podcast. I'm absolutely delighted to have the opportunity to discuss our areas of interest and expertise related to infections and vaccinations for MS patients. My area has been studying the infections of the nervous system since the beginning of the AIDS pandemic, and over the years and decades, we've developed expertise related to various types of CNS infections. That includes ones that are developing in individuals who have immune compromise due to a variety of different reasons. Dr Berkowitz: Fantastic. Well, glad to have the opportunity to speak with you today. When I was in medical school---and you were my attending, actually, we were just reminiscing, which we probably think was not that long ago, but is now over twenty years ago---there were just two medications for MS, right? Beta interferon and glatiramer acetate. And now we have over a dozen, and it's amazing to think of all the progress in these last two decades, as well as for related diseases like NMO. I don't think we even had the aquaporin-four biomarker, right, when I was working with you as a med student in the early 2000s. Dr Nath: And that certainly dates me a lot. Dr Berkowitz: Both of us. Dr Nath: Yeah. Dr Berkowitz: Of course, with all these new treatments, these have been amazing advances for our patients, right? But these come with new treatment-related risks to monitor for with the immunomodulatory medications for MS and related disorders. And one of those most important risks is that of infection. So, your article reviews the potential infectious complications of medications used to treat MS, NMO, etc, and also covers considerations related to thinking about vaccines in this patient population. So, as the MS treatment landscape grows, I can say as a general neurologist, keeping up with all these medications and what to screen for and what to worry about and when to vaccinate just becomes more challenging every year. And your article has so many helpful tables, some organized by medicine, some organized by- sorry, medication, some organized by infection, some by vaccines. So, this is gonna be a great resource for our providers to print out and tape up in their clinic rooms. We won't be able to get into all the depth and detail that you have in this article today, but I do want to focus on some of the key points here related to the common medications we use for MS and which infections to think about and which vaccine considerations we might need to keep in mind for these medications. But before we delve into the drugs, I just wanna ask you more broadly, you talk in the article about the challenge of patients with immune-mediated diseases who are on immunomodulatory therapy being at risk for both flares of their disease and for infections; and these infections can present somewhat atypically, right, in immunomodulated hosts, to maybe coin a term you can correct me on, because they can't mount the full inflammatory response. So how do you approach new symptoms in patients on these immunomodulatory medicines as far as distinguishing disease flare from a treatment-related infection? Dr Nath: So, I have to say that although a lot of new treatments have come along for MS, and they've really, you know, improved the outcome tremendously and there are so many different options, it has also kept people like me relevant because they cause a lot of various types of infections, and so keeps me in business all the same. But just as you mentioned, there's so many of them, even I have difficulty keeping track of what does what. So, you do need to be able to refer back to published literature, and the tables, I hope, will be quite useful in that regard. You're absolutely right, and you can get new infections, you can get reactivation of existing infections, and you can get atypical presentations of various types of infections that you may not normally think of. So that presents multiple challenges to the treating physician. The other interesting thing about MS is, just as you mentioned, that you already have CNS lesions to begin with. Now, on top of it, you have an infection, so now how to sort out what is the existing disease and what is the infection, it can again become challenging. But one thing is for sure: all these infections are caused by an organism. So, what you really need to do is, the underlying diagnostic is to demonstrate the presence of the organism. Whether you demonstrate it depending on the infection in the spinal fluid or in the brain or, you know, some peripheral organ system, that is going to be key to making the diagnosis. So, all your clinical acumen is good, but that alone may not be sufficient. Dr Berkowitz: Very good. So, when you see a, a patient now who has a new neurologic symptom in the context of an immune-mediated disease who's on immunomodulatory therapy, what goes through your mind? Are you thinking this disease and this drug, and sort of what are the infections, and does the syndrome match? Or are you thinking, you know, you can't always rely on the imaging to distinguish between, say, a flare of an MS and PML because white matter lesions could look similar? How do you sort of approach this scenario when it comes up? Dr Nath: So, you're right. You have to keep an open mind so that even though you know some infections are more likely to occur with certain types of medications, that doesn't mean that others cannot occur. So, I think when you first see the patient, you should not jump to conclusions, but rather have an open mind. But yes, for example, your patient is on natalizumab, the chances of PML are going to be high. It's a very interesting drug. It does not cause immune compromise in the periphery, but what it's doing is preventing these cells from getting into the brain. So, because then it's acting at the blood-brain barrier. So that means that organisms that are already present in the brain have an opportunity to get reactivated. Turns out you don't have a lot of organisms in the brain, except JC virus seems to be one of them that does somehow, in some individuals, manage to reside out there. And so that can get reactivated. It can get reactivated in the periphery and then enter the brain, too. So, where the very specific mutations have to occur in that virus in order to take residence in the brain. That would be a suspicion that you might have, and MRI can be useful in, again, helping you think about that possibility. If you have typical lesions involving the U fibers, they're demyelinating, usually you do not have much edema around them because patient is immune compromised, but certainly within the brain in these individuals. And so, then you need to demonstrate the organism. The demonstration of the organism should be in the spinal fluid and not in the blood because in the virus, it can-- is reservoir in the kidneys and in the lymph nodes, and periodically it'll shed into the blood. Detection of the organism in the blood can be a false positive, but in the spinal fluid, it shouldn't be there unless you have an infection. Or if you cause a traumatic tap, I guess, if a patient is viremic, that's a possibility, but those are extremely rare. So at least for PML, that's the way that you would diagnose it. Now, you can develop, for example, if an individual is on fingolimod, you can get a wide variety of infections. Here it's a totally different type of mechanism of action. Here the cells are trapped within the lymph nodes, so that means now your entire periphery is immune compromised, right? So here you can get viral infections, bacterial infections, fungal infections. So here, if a patient presents with new neurological symptoms, you have to have a really open mind for all these possibilities. Now, let's say a patient was on dimethyl fumarate, and dimethyl fumarate causes neutropenia early on. So here you have to worry about an individual developing bacterial infections, so latent tuberculosis or bacterial meningitis can occur in these individuals. That's something to keep in mind. It's not that other infections cannot occur with dimethyl fumarate, you can see PML and other things too, but the chances of bacterial infections are greater. So, you got to make sure that you draw all the cultures for that purpose. Similarly, if you're on a complement inhibitor, like a C5 inhibitor or the thing that I could use in NMO, there are the chances of meningococcal meningitis. So, these patients, you need to prevaccinate them before you start these kinds of treatments and look for that possibility. When you suspect bacterial infections, particularly acute bacterial meningitis, there time is of essence. Also, in some of the acute viral infections, for example---herpes encephalitis is another one---you have to be so careful, and if you suspect any of them, even if they're with possibly atypical manifestations, you treat first and then diagnose later, and draw all your cultures, whatever you need to, and just treat them. And these infections can also cause cerebral edema, so one has to be careful about doing spinal taps in these individuals. You want some kind of neuroimaging before you do them. In the days when we didn't have neuroimaging, we used to say, "Okay, if your patient has focal neurological signs or is comatose, you don't do it." But these days, you can get imaging very quickly and very easily. All the-- Because of our stroke management, we've learned how to do them so quickly. So, I think there's little excuse not to do imaging and prevent herniation from occurring. Dr Berkowitz: That's very helpful. So, using the information we know about the drug, and we're going to rapid-fire review some of that in a bit to know what infections the patient is susceptible to, but acknowledging that any patient can get any infection, right? Whether they're on particular medications or not. And then if you're not sure, based on the neuroimaging, which as you said, is helpful, but not always helpful in distinguishing between infections and flares or, as you said, in the case of meningitis, encephalitis, early on at least, especially in immunocompromised or immunomodulated, quote unquote, patient might not see the typical imaging. So really, when safe, getting CSF or cultures, PCRs, and other infectious studies too is really gonna be the definitive diagnostic maneuver here. Is that fair summary across the board? Dr Nath: I think you said that absolutely right. And you summarized that correctly. And, you know, thing about infection, a lot of neurological diseases are, you know, diagnosed by clinical acumen, like your Parkinson's and Alzheimer's and others. Think about infections is caused by an organism, demonstrate the organism, right? That should be your goal. It doesn't mean that clinical acumen is not important, but here you have an opportunity to demonstrate the organism, so you should depend upon that. Dr Berkowitz: Okay. Well, you gave us a nice segue by talking about some of the infections to worry about with some of the medications. So what I'd like to do now for the sort of second half of our interview here is to go through some of the more common medications used for MS, and if we have time, for NMO, and just sort of go kind of rapid fire here, and for each medication, if you can tell us the kind of top infectious concerns and whether when to consider them or what screening needs to take place before or during administration of the medication, and then any vaccine considerations we should be aware of. Some of these will obviously be quite short depending on the medicine. So, going back to the two medications I alluded to earlier that were the only ones in play when you and I last saw each other on the wards when I was a medical student, beta interferon, glatiramer acetate, any infections or vaccine considerations with these medications? Dr Nath: No, I think they're probably your safest medications now as far as immunomodulatory therapies are concerned. These two, and IVIG, if you ever use them, are probably the safest, do not require any vaccine considerations, per se. Dr Berkowitz: Perfect. Okay. So, moving on to fingolimod and others in the sphingosine-one phosphate receptor modulator family, what are the infectious considerations? Any prescreening or vaccination considerations? Dr Nath: I think all your patients should be prescreened for antibodies to JC virus, because there is a risk for PML, and those who are positive should be closely monitored. So, it's not an absolute contraindication for using these medications, but they just require closer monitoring. With this class of drugs, PML is of consideration. Also, these varicella-zoster virus infection, yeah, with that you can develop zoster encephalitis or myelitis. It can present with motor symptoms as well, which can be atypical. You don't usually see them otherwise in immune-competent individuals. So, varicella-zoster, sometimes you can develop encephalitis, also vasculitis with varicella-zoster, so one has to be careful. So, getting the shingles vaccine can be actually very helpful to prevent these things. And then some patients can even develop herpes simplex encephalitis also, and that can be extremely atypical. So, they don't- they can involve the basal ganglia, can involve the brain stem and cerebellum. So again, your index of suspicion should be very high. Interestingly, although HSV encephalitis has been associated with NMDA receptor encephalitis, those reports of NMDA receptor encephalitis have not been published yet with NMS patients. Not sure why, maybe they just have been missed. But that doesn't seem to be a major concern. And then there are a whole host of other infections that can occur with this class of drugs, and that can include toxo; fungal infections, particularly crypto. There's a case report of histoplasmosis; hepatitis virus, particularly hepatitis C; and then the poxvirus is a good example. You can get molluscum contagiosum; warts with papillomavirus; you can get atypical mycobacteria; and even Kaposi sarcoma, which is HHV8. So, there's a huge variety of infections with the sphingosine one phosphate receptor modulators. Dr Berkowitz: And any- aside from screening for JC virus before initiating these, any- and then continuing to monitor for JC antibody index, any other considerations as far as labs to send, monitoring before or on the drug or vaccine considerations for patients on fingolimod and the others in this category, siponimod, etcetera? Dr Nath: Yeah, there are a lot of things to consider. All the details are really available in the chapter if you look at them. But briefly, all the things that one could potentially vaccinate patients for, all these infections I mentioned, one should do so. The timing is critical so that if you can do it before treatment, I think, before starting treatment, that is absolutely important. And you got to give them at least, you know, two to three weeks for these vaccines to take effect before starting your medication. If your patient already arrives on a medication, then you got to play this game of you know, before the next dose, give them again two to three weeks before the next dose and start vaccinating them and get all the vaccines in. Broadly, about the things to worry about the vaccines are you have live vaccines, and you've got the inactivated vaccines or the subunit vaccines. You have to be careful with live vaccines, because if your patient is immunocompromised, that virus can sometimes itself cause harm. For example, you know, yellow fever is one, and there you can develop encephalitis from it. Measles, mumps, rubella, these are all live vaccines. Now, the good thing is that a lot of us have been immunized very early in childhood, but that may not be the case any longer. And so, these things, one has to be very careful with when you're giving live vaccines, that we want to avoid them as much as possible, and individuals are gonna be immune-compromised. But all the others, meningococcus, for example, you should- the HPV vaccines, the varicella zoster vaccines, all these things, you've got to pre-vaccinate and make sure that they have an antibody response to them before starting immunocompromising therapy. Dr Berkowitz: Perfect. Okay, moving on to some of the other orals. What infectious and/or vaccine considerations do we have with teriflunomide? Dr Nath: Okay, yeah. Teriflunomide is a very interesting drug. It's relatively safe. There is concern about the possibility of varicella zoster infection, people have reported that, and also tuberculosis. But PML is extremely rare, if not at all, and we haven't seen herpes encephalitis quite yet. Dr Berkowitz: Got it. How about dimethyl fumarate? Dr Nath: Yeah. So dimethyl fumarate is... as I mentioned earlier, it's interesting because it causes this neutropenia. It's transient, but it occurs early on, and these patients can be at risk of PML, although small. They can develop varicella zoster virus infection, herpes encephalitis, and also fungal infections. For example, cryptococcal infection has been reported with dimethyl fumarate. Dr Berkowitz: Okay. We've spoken a bit about natalizumab and PML, and you have extensive information on this in your article, and I'll defer the reader to that. But for natalizumab, what are the key points every neurologist should know about natalizumab and PML as far as from the practical perspective, screening, frequency of screening, when to worry, when to not use natalizumab at all in the first place based on what you find in your screening for JC virus? What are the key points every neurologist should know? Dr Nath: Uh, yes. You bring up an important point, and that is all patients should be monitored for JC virus. If they're JC virus-negative, so that's your most ideal patient to go on natalizumab, but that doesn't mean they cannot get infected with the virus. In fact, there's an interesting study claiming that, you know, patients, when they get these infusions, they're all sitting in the same room getting infused. Some have JC virus, some don't have JC virus, and so there's the potential that we may be aiding the transmission here in some way or another. The virus is an interesting one. It comes out in urine, and then it's spread through oral contamination, gets into the tonsils, and then spreads from there to your marrow and resides in the kidney and the marrow, as well as the lymph nodes, forever. So, you, you have to monitor these patients to see that during the course, even if they're negative, they could turn out positive. So, every six months or a year, an antibody test should be done on all patients irrespective. If a patient already has antibodies, that's not an absolute contraindication. It just means you've got to monitor them closely for development of new symptoms, and if, whenever there are new symptoms, don't just assume this is due to MS, but just make sure the MRI is done with and without contrast. The- and if there's still a suspicion, that you do a CSF evaluation for JC virus. Just detecting, looking for JC virus in the blood, a rising titer is another thing that can help you. And so, the titer is also important. And the reason you have rising titers is it means that there's an infection that's already occurred in the brain, and the immune system is reacting to that infection by increasing titers. But that alone is not sufficient to make the diagnosis. You still- that gives you an index of suspicion. You've got to then do the MRI and the spinal tap to, you know, be absolutely certain. So, each patient is a little bit different, so the way you monitor them is going to depend on where they are. You know, if they've had prior immunomodulatory therapy before starting natalizumab, or if they're on natalizumab for more than two years, then the chances of PML are much greater, so you may want to monitor them more closely. Uh, they never had any prior immunomodulatory therapy, you're just starting natalizumab, maybe once a year is sufficient. So, I think you've got to tailor it depending on what your risks are for each patient. Dr Berkowitz: Perfect. That's very helpful. And again, you write extensively about PML and natalizumab and PML considerations in your article. So, for a more detailed and in-depth discussion of what we just discussed, definitely hope readers will take a look at your article. Okay. Last but not least---certainly not least, 'cause we're using these probably, it seems, the most commonly in many places I've worked---rituximab, ocrelizumab are B-cell therapies for MS. What are some of the infectious and vaccine considerations related to these infusion medications? Dr Nath: So, there's concern for PML with anti-B-cell therapies also, maybe not to the same degree as natalizumab, but the same principles should be applied. A lot of people think that these are relatively safe. I don't think so. I think we see enough number of patients on B-cell therapies with PML. So, I would use the same caution because these infections are... you know, can be fatal. So, one should be very careful, even with anti-B-cell therapies. And just with natalizumab, you also have the risk of VZV infection causing shingles. HSV1 has been reported, but there's another interesting complication that has been reported with anti-B-cell therapies, and that is severe West Nile encephalitis. And as mosquitoes-borne diseases are getting more and more prevalent, and we're seeing West Nile cases erupting every summer, I think one's got to be, you know, very cognizant of the fact that this can occur. These patients should take precautions to prevent mosquito bites from occurring and not expose themselves to areas where they could be at risk for it. Unfortunately, there is no vaccine for it and no specific treatment for West Nile. So, all one can do is use prevention strategies for mosquito bites. Dr Berkowitz: Yeah, I'm glad you mentioned that. I think the only really truly severe neuroinvasive cases I've seen of West Nile virus have indeed been in patients who were being treated with B-cell therapy. Not, if I'm remembering correctly, for immune-mediated disease, but for a lymphoma, so probably other confounding factors there. But yeah, it's a disease we learn about and think about, but I've only seen the most severe cases in patients who had abnormal immune systems, so I'm glad you flagged that. This has been a very helpful discussion, and I've learned a lot from you. I learned a lot from your article, just as I did when you were my attending some 20-something years ago on the wards when I was a medical student. So, it's good to continue learning from you through your writing and research, and today from getting to talk to you again. I encourage our readers to read your article and to bookmark those tables for when these considerations come up for your patients on these immunomodulatory therapies and you're wondering which infections to worry about and how to manage vaccines in this patient population. So again, today I've been interviewing Dr. Avi Nath about his article on vaccine considerations and infection risk in multiple sclerosis and related disorders, which he wrote with Dr. Amit Bar-Or. This article appears in the April 2026 Continuum issue on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues, and thank you again to our listeners for joining today. Dr Nath: Thank you so much, Aaron, for that wonderful interview, and I'm extremely proud of all your accomplishments over the last 20 years. You've done an amazing job, and it was such a pleasure to see you and to be able to do this interview with you. Thank you again. Dr Berkowitz: Thanks. That means a lot. I never would have imagined- we won't say 20, how many, but 20-something years ago as the medical student looking up to you and all your expertise on these infections and all of your research that led to so much of our understanding on these, that I would find myself interviewing you two decades later. So, for all the students listening, you never know where you'll end up, but I appreciate your very kind words. Dr Nath: That's what we hope for all our students. Thank you so much. Dr Berkowitz: Thanks again. Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
Why is brain cancer so hard to detect and treat - and what if we could change that? In this episode of Rx for Biotech, host Chris Leidli sits down with Marc Hedrick, CEO of Plus Therapeutics, and Russell Bradley, General Manager of CNSide Diagnostics, to explore a new, integrated approach to treating some of the most challenging cancers in medicine: central nervous system (CNS) cancers, including glioblastoma and leptomeningeal metastases. Brain and CNS cancers are among the most difficult to treat because of the blood-brain barrier, which prevents most drugs from reaching tumors. In fact, only a small percentage of therapies can effectively cross into the brain—limiting treatment options and outcomes. Plus Therapeutics is tackling this problem with a novel approach using targeted radiation therapy delivered directly to tumors, bypassing the blood-brain barrier. Their lead program uses a radioactive isotope (rhenium-186) delivered via nanoliposomes, allowing high doses of radiation to reach the tumor while minimizing damage to the rest of the body. At the same time, CNSide Diagnostics is helping physicians detect cancer earlier and monitor treatment response using an advanced cerebrospinal fluid (CSF) diagnostic test. This highly sensitive test can identify even small numbers of tumor cells—helping doctors make faster, more informed treatment decisions. Together, this combination of diagnostics + therapeutics + data represents a new model for precision oncology and personalized cancer care. In this episode, we discuss: • Why brain cancer is so difficult to treat • The role of the blood-brain barrier in limiting therapies • How targeted radiation therapy can improve outcomes • The importance of early detection and diagnostics • How monitoring tumor cells can guide treatment decisions • The future of integrated cancer care (theranostics) This conversation offers a powerful look at how innovation in both treatment and diagnostics could help improve survival and quality of life for patients with some of the most aggressive cancers.
Although rare, recognizing NMOSD is crucial for improving patient outcomes through correct diagnostic and treatment approaches. Reports of atypical forms and increasing knowledge of clinical, imaging, and laboratory-specific features are fundamental for the accurate recognition of this condition. Research on targeted therapies and biomarkers measuring and predicting disease activity will improve NMOSD management. In this episode, Gordon Smith, MD, FAAN, speaks with Sara Mariotto, MD, PhD, coauthor of the article "Neuromyelitis Optica Spectrum Disorder" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Mariotto is a neurologist in the Neurology Unit in the Department of Neurosciences, Biomedicine, and Movement Sciences at the University of Verona in Verona, Italy. Additional Resources Read the article: Neuromyelitis Optica Spectrum Disorder Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: Neurology is an increasingly therapeutic specialty, and across many of our subspecialty areas, lots of new drugs are being approved. Are you interested in learning more about a historically disabling disorder for which we now have a spectrum of new therapies that, if used appropriately and promptly in the right clinical situation, promise to dramatically improve patient outcomes? If so, keep listening. My name's Dr Gordon Smith. Today I'll be talking with Dr Sara Mariotto about her article on neuromyelitis optica spectrum disorder or NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 Continuum issue on multiple sclerosis. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today, I'm interviewing Dr Sara Mariotto about her article on neuromyelitis optica spectrum disorder or NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 Continuum issue on multiple sclerosis. Sara, welcome to the podcast, and maybe you can start by introducing yourself to our audience. Dr Mariotto: Yes. Thanks, Gordon. I'm Sara Mariotto. I'm a neurologist, and I work at the Neurology Unit, University of Verona, where I do both clinical diagnosis and research into neuroimmunology---so, in particular, autoimmune encephalitis, NMOSD, and MOGAD. Dr Smith: Well, this is a super exciting area. Whenever I hear about NMOSD, I think of one specific patient I had, and I always think of her when I come across something like your article, which is really fantastic. So, before we dive into the details, I wonder if maybe you can just explain to our listeners who aren't up to speed on what NMOSD is, what the disorder is, and maybe why it's so important that all of our listeners learn how to recognize it quickly and get people started on therapy. Dr Mariotto: Yes, sure. So, neuromyelitis optica is an inflammatory autoimmune CNS disorder usually associated with aquaporin-4 antibodies, although there are a few cases, around 10%, who can be antibody-negative. And I think it's very much important to have in mind this disease and recognize it because it can be severe, as you pointed out; can present with very severe optic neuritis, myelitis, the brain stem, or area postrema syndrome. So, it can be really severe, affect quite young people around 40 years of age---although it can affect also the pediatric population and elderly people---and, importantly, it can be treated. It's very much important to treat this patient in the acute stage very quickly with steroids or plasma exchange in addition, and then to start a chronic treatment. So, we have treatment for this condition. So, it's very much important to, to recognize it quickly and treat the patient properly. Dr Smith: So, I wonder if we can talk a little bit about the diagnostic criteria and boundaries of NMOSD, right? So, someone who comes in with bilateral op- severe long segment optic neuritis or long segment myelitis, we think about it. But what are the boundaries? Should we be looking for this, for instance, in someone who comes in with a unilateral optic neuritis or looks like typical multiple sclerosis? Is it important to get aquaporin-4 antibodies in those patients? What do the diagnostic criteria say about this? Dr Mariotto: So, I wouldn't test aquaporin-4 antibodies in all patients with demyelinating conditions because although aquaporin-4 antibody assay is very specific, as for all assay and all antibody testing---also for MOG antibodies, for example---some false positive results can come out. So, I would suggest to test aquaporin-4 antibodies not in typical MS cases but in those who could be suggestive for not being MS, so in all those cases with atypical optic neuritis and myelitis or other syndromes. For those cases, it's important to test aquaporin-4 antibodies, but I wouldn't test them in all typical, classical MS cases. As I said, it's quite specific, the assay, so it's uncommon to have false positive results, but it can be. Dr Smith: Serum, CSF, both? Dr Mariotto: So, for aquaporin-4 antibodies, they're usually present in serum. They can be positive also in the CSF. And there are a few reports of isolated CSF positivity. But if we analyze larger samples volume, then it becomes clear that isolated CSF positivity is so, so rare that it's not recommended to test them in the CSF when serum is negative. So, for aquaporin-4 antibodies, the recommended matrix of testing is serum, which is different for MOG, which is not the topic of our article but is important to mention because MOG antibodies should be tested in serum and CSF. But aquaporin-4, I would recommend to test serum. Dr Smith: What are the boundaries between MOGAD and NMOSD? And you talked about the differential testing of antibodies, which I was going to ask about. But when should we think of NMOSD relative to MOG? Dr Mariotto: Yeah. There are aspects which are the one mentioned in the criteria, highly suggestive for NMOSD. But the clinical spectrum can be similar to that of MOGAD. Usually, although there are some clinical aspect---like, for example cortical encephalitis or ADEM, which is more typical for MOGAD, or others like area postrema syndrome, which are more typical of NMOSD. The spectrum can be similar among the two conditions, so that's why in our clinical experience, usually they ask both aquaporin-4 and MOG antibodies in patients. It's- for experts, it can be easy to differentiate the two conditions, but for nonexperts can not be so easy. Dr Smith: Can you define area postrema syndrome? I think not all of our listeners see that every day. Dr Mariotto: Yeah, sure. This is a syndrome which is highly suggestive of NMOSD. That's why I mention it. And it's characterized by nausea, vomiting, hiccups are known as the syndrome. And it is very, very suggestive because of the expression of aquaporin-4 in that area of NMOSD. That's why I strongly recommend for all patients who comes out to have this syndrome to test for aquaporin-4 antibodies. MOGAD is hardly ever positive for that, so I think that whenever you see a patient with that syndrome, you should think about NMOSD. Dr Smith: I'm just curious, aquaporin-4 is a water channel, which is kind of an interesting concept. Our conversation, I really want to make sure we give clinically important information to folks, but it's so curious to me at least, how does this actually result in a inflammatory demyelinating syndrome? For a simple neuromuscular guy, what's the immunopathogenesis of this? Dr Mariotto: Yeah, the immunopathogenesis is quite complicated, as in all CNS disorders. And of course, aquaporin-4 antibodies are the main focus, but they are not the only one. As you said, aquaporin-4 antibodies have a target, this water channel, which is at the basis of the disease, and they are produced by the interplay between T cells, B cells, and plasma cells. But then also eosinophils, macrophages, cytokines, and chemokines are involved, enter the CNS, and then another important component is complement, which is highly activated in this disease. At the end, we have astrocyte damage because astrocytes are the main target of the disease, but also axon and myelin are involved. So, it's a quite complex pathogenesis based on the antibodies, but not only on that. Dr Smith: And this will become important when we start talking about treatment. There seems to be a recurring theme of long segment demyelination, right? Optic neuritis is typically a large percentage of the length of the optic nerve, and obviously the myelitis se- more than three segments. Do you see other long segment areas of CNS demyelination, corpus callosum or things like that? Any ideas why that is, if that's true? Dr Mariotto: Of note, this is quite interesting because usually when we have NMOSD, we have a longitudinal involvement, especially of the optic nerve and spinal cord, while brain lesions are quite different. Like, we usually do not have the typical Dawsen fingers-like lesions that we have in MS, for example, or the classical periventricular or subcortical extensive lesions that we can see and we have in mind when we think about MS. In some cases with NMOSD, the brain is completely negative, so we do not see anything. And Dawsen lesion's quite suggestive of NMOSD. So, you're right. I mean, this is related partially to the expression of aquaporin-4, and that's why we have this typical involvement also for area postrema, for example, and maybe also our other examples of clinical aspect that we can see in these conditions. But it's basically linked with the expression of aquaporin-4, which is the main target of the disease. And that's why usually the brain doesn't show so much involvement as we can see in MS, for example. Dr Smith: I was actually really interested in some of the unusual manifestations or phenotypes, and I don't want to get into arcadia, really, but which of these should our listeners be familiar with that would really suggest that they should be thinking about NMOSD beyond the area postrema and other features that we've already talked about that are part of the core criteria? Dr Mariotto: Yeah. I mean, I think that the encephalic syndromes or also ADEM, which is most typical of MOGAD but can be observed also in NMOSD or PRES, for example, are syndromes that can be considered in patients with NMOSD. There are the typical ones, which are the ones showed in the criteria, but whenever we have a brainstem involvement or, like, these encephalic syndromes or also PRES, we should think about NMOSD also. Dr Smith: Another area I was interested in are red flags. In your article, you talk about red flags that might suggest an alternative diagnosis, right? And then this presumably is particularly important in seronegative patients, which 10% is not a reasonably high number, I suppose. What are red flags we should be thinking about for some other diagnosis? Dr Mariotto: Yeah. I would here mention two very important red flags. The first one is a very hyperacute onset. Usually these conditions, these inflammatory conditions have a subacute onset, so whenever you have a very, very acute onset, you should think about something else. This can occur sometimes also in NMOSD, but hardly ever occur. Like, a very acute myelitis, the first thing we should think about is a vascular origin, for example, with a lot of pain and not about NMOSD, although sometimes the differential diagnosis is not so easy. The second thing is a progression independently of relapses, which hardly ever occur in NMOSD. Usually in NMOSD, we have the onset, and then we have a relapsing disease course. That's why we have to treat patients always and not to stop treatment. But we do not have progression in the meanwhile, while we can have, for example, this in MS. Same thing is for MOGAD. So, these are two things that I think is very much important to keep in mind. Dr Smith: I want to pivot to talk about treatment because that's been super exciting. But rumor has it there are new diagnostic criteria coming for NMOSD in the next year. I bet you know a bit about those. Can you give our listeners any indication about kind of where the puck is going on this? Not so much what the criteria are specifically, but what sort of diagnostic challenges are the new criteria going to help us with once they come out? Dr Mariotto: Yeah. So basically, we are working on that, so you will read them in the next future. This is the good point of the conversation on the new criteria. And we work a lot on the definition, on the new definition and nomenclature of NMOSD; on the definition of seronegative NMOSD, which is also quite tricky; and then on the assay we should use to test aquaporin-4 antibodies, and also on potentially new syndromes which should be included into the main feature of the disease. But hopefully you will read about this very soon. Dr Smith: Looking forward to it. And Continuum Audio listeners, you heard it here first, so thank you. Let's pivot to treatment. This has been super exciting, and I wonder if the way to approach this is to start with acute management and then sort of chronic management. Would that make sense? Dr Mariotto: Sure. Dr Smith: Let's say I go on service on Friday, and I have a patient who comes in with positive aquaporin-4 and bilateral optic neuritis. What's the acute approach to managing that patient? Dr Mariotto: So, the first approach is to administer intravenous steroids, but I would not wait to escalate to plasma exchange. There is quite good evidence that we should treat the patient with additional plasma exchange very quickly, and every day of delay of plasma exchange can cause increased disability. So, we should treat patients with steroids first, and then if we are not satisfied by the recovery, soon start with a plasma exchange. There is also some evidence, although less, for IVIG, but it's important to try to treat them very quickly, even if it's Friday, you know, there is the weekend and so on. But I think it's very much important to start with steroids after excluding other infectious causes or so on, and then to start quickly with plasma exchange. The main problem could be that we do not have the results of the antibody yet. Dr Smith: Right. So, let me ask that question. You know, let's say my patient comes in on Friday, and clinical syndrome that really looks like NMOSD, and we're waiting for the aquaporin-4. There are many places where it's hard to get plasma exchange over weekends. And so, in that setting, are you better off doing the steroids over the weekend then PLEX on Monday, or should we just give IVIG because maybe it's as good as PLEX? What's your advice there? I'm trying to get ready for Friday because I know one's coming in. Dr Mariotto: That's true, that's true. Usually they come on Friday or Saturday. I think it's acceptable to have three days of steroids and see how the patient improves, and then after three days to start with plasma exchange. Actually, we have a very good improvement if we start between three and five days after onset. So, I think waiting for three days is acceptable just because we can see if the steroids work properly or not, and then we can quickly start to plasma exchange. But I would not wait, like, 10 days, you know, before starting with a plasma exchange, and I would not wait for antibody results. Dr Smith: Got it. Super helpful. And I'm actually not joking around, I learned recently that I have a reputation among our residents for having lots of optic neuritis when I'm on service, which I think is sort of karmic justice for being a peripheral nerve expert. But let me ask another question. So, let's say we do that, and the patient gets three or five days of pulse methylprednisolone and five courses of PLEX, and they're not doing well. Do you then just move right along into another agent B cell depletion therapy? I mean, what's your next step in escalation in the acute setting? Dr Mariotto: I would for sure start to, as you said, with steroids, plasma exchange, and in case IVIG, and then quickly move to chronic treatment. And for patients who are not recovering well, I would think of something which has a quick effect so we can really start treating patients very quickly. There are different options. And all over the world, there are different rules for using immunosuppression in NMOSD. Like in Italy, for example, it's different from US or other countries, Germany, for example. There are different approved treatments and different rules of using them before or after rituximab, for example. We all know that there are treatments approved for NMOSD all over the world. But in some countries, like for example in Italy, we should use rituximab first, and then if it doesn't work, escalate to the approved treatment. I know in the US it's different. But anyway, for a patient who does not improve quickly, I would start with something which has a quick effect on the disease. Dr Smith: And then rituximab versus inebilizumab, you know, CD20, CD19, what's your advice there? Is one preferable to the other, you know, if we have options to do either? Dr Mariotto: Yeah. So, between rituximab and inebilizumab, we know that the target, well, is different, but is anyway B cells, so CD19 and CD20. With CD19, we can affect both plasma blast, plasma cells, and B cells. That's why the target is broader. And of note, this is an approved drug, while rituximab is, in most countries, used as off-label treatment. Dr Smith: So inebilizumab would probably be preferable if we're able to do that. Dr Mariotto: Unfortunately, there are not so many studies comparing rituximab with the approved drug, which is, of course, a pity, but that's the case. While we have clinical trials for all the approved drugs, and although the trials were designed differently, as we mentioned in the Continuum paper, we can argue something of the comparison between the approved drugs. But it is not so clear the comparison between rituximab and the new drugs, which is also something that we should work on. Dr Smith: And then for chronic suppressive management, what other options are there? Dr Mariotto: So, in addition to B cells, target can be interleukin-6, as we know with tocilizumab or satralizumab, and then complement with eculizumab. These drugs are both based on the pathogenesis of the disease. That's why we also discuss it in the paper, which shows a clear involvement of complement, and among cytokines of interleukin-6. So, targeting these made clear that could improve the disease quite well, and that's why they designed some clinical trials on these drugs, which are now approved, as we said, for NMOSD. Dr Smith: Wow, so many options, and a lot of questions, but limited time. Let me just ask a couple of more. I see a lot of myasthenia patients, and there's a lot of variability, as you know, in patients with myasthenia, the extent to which complement is an important mechanism versus other, you know, important mechanisms. To what extent is response to a complement inhibitor kind of uniform across NMOSD? Or there's some patients who just don't respond to a complement inhibitor and others that respond really well. And then just, I'll just give my second question out is, you know, what about combination therapies for patients who have particularly challenging NMOSD? Dr Mariotto: So usually these patients have a terrific response to complement inhibitors, and this is also shown by the clinical trials where we saw how eculizumab have a very impressive effect on the disease. And also, maybe this is also your experience, a very quick effect. So that's why there are also thoughts on using it in a very acute stage of the disease. That was what I was thinking about before. But then it has a very huge effect on complement, which is a major factor involved in the pathogenesis of NMOSD also in the chronic disease stage, and that's what also we see from clinical trials. Usually, we prefer to switch treatment from one to another and not to combine them. Of course, in very difficult cases, this can be considered, but the recommendation is to switch from one of these approved drugs to the other, or from rituximab to one of the approved drugs, and try to find out the best for our patient before combining them. Dr Smith: The complement inhibitor trials are breathtaking, at least for me. If I'm trying to convince students to go into neurology, I'll say, "Take a look at that paper," because anyone who claims that we're "diagnose and adios" is so wrong. It's so exciting. So, at a high level, this must have fundamentally changed outcomes for patients. I mean, it's still a difficult disease, but what is the kind of prognosis for that patient I described who comes in, gets the therapy you talked about? What does their long-term outcome look like in this modern therapeutic environment? Dr Mariotto: So, NMOSD is almost always a relapsing disease. That's why, as we mentioned, we have to treat patients always. But the prognosis changes a lot since we were also able to use all these drugs for the disease. So, the prognosis changes if we recognize it properly and early, and if we treat NMOSD properly with immunosuppressives. So, whatever we choose it's important to start it quickly, and this is the only way that we have to improve the prognosis of this disease. We have very active cases, but we have also cases who responds quite well to this immunosuppressive treatment, since now we have, as mentioned, these ones which are very impressive and show incredible results. So, the prognosis of the disease change in the last year, thanks also to the improvement of the diagnosis and of the treatment choices for the disease. Dr Smith: I'm just... I- maybe my last question, you know, just at a personal level, not only for you as an expert who's caring for these patients, but in the patient community, this must have been a pretty exciting period of time, right? I mean, these, these drugs are coming fast and furious, and what a change. What's the kind of zeitgeist in the community, both your professional community and amongst the patient community about where we are? Dr Mariotto: Yeah, you're right. The last years were defined the years of NMOSD and also MOGAD because we had finally approved drugs which is relevant for all the disease that we treat and changed the landscape of the disease for clinicians, but also for patients. And we have more than one, as we said, so we have more options that we can also discuss with patients to try to choose the best one in terms of activity, but also route of administration or time. Some years ago, we just had rituximab, which is not approved in most of the countries, and now we have different approved drugs. And we improved the diagnosis of the disease thanks to the availability of live cell-based assay. And then we are working a lot also on biomarkers like GFAP, for example, which has been shown to be a very attractive biomarker able to mark disease activity and maybe also prognosis on this disease. So, you're right. I mean, in the last years, the landscape of NMOSD changed a lot. Dr Smith: Sara, thank you so much for talking with me. I could keep going for another half an hour, but I would be in trouble with my editor, so I think we probably need to wrap it up. But thank you so much. This has been very informative. Dr Mariotto: My pleasure. Dr Smith: Mine too. Thank you. Again, today I've been interviewing Dr Sara Mariotto about her article on NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 issue of Continuum on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues, and thanks to you, our listeners, for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
Spinal cerebral spinal fluid (CSF) leaks are significantly more common in those with connective tissue disorders than many realize, yet patients often suffer for years before finding the right diagnosis. In this episode, neuroradiologist Dr. Andrew Callen joins Dr. Linda Bluestein and co-host Dr. Knight to discuss the complexities of CSF dynamics and the challenges of diagnosing leaks when routine imaging appears normal. Dr. Callen explains the different types of leaks, including the elusive CSF-venous fistula, and why common clinical assumptions, like the requirement of a low opening pressure, are often incorrect. From the Bern Score to the critical differences between Chiari malformations and positional brain sag, this conversation provides an essential roadmap for patients and clinicians navigating the "unseen" world of intracranial hypotension. Takeaways: Cerebral Spinal Fluid Basics: CSF is a clear fluid that cushions the brain and spine and plays a vital role in metabolic function. Three Major Leak Types: Leaks can occur via bone spurs poking the dura, nerve root tears (common in EDS), or CSF-venous fistulas where fluid drains into the bloodstream. Atypical Presentation: While "orthostatic headaches" (worse when upright) are classic, many patients experience vestibular symptoms like ringing in the ears, muffled hearing, imbalance, or cognitive "brain fog". The Pressure Myth: The vast majority of proven CSF leak patients do not have low opening pressure; it is a disease of low volume, not necessarily low pressure. Chiari Misdiagnosis: Positional "brain sag" can look identical to a Chiari malformation on imaging, leading to inappropriate surgical treatments if not carefully evaluated. The Bern Score: This probabilistic scoring system based on MRI findings helps radiologists determine how likely it is that a myelogram will successfully find a patient's leak. Imaging Strategy: Clinicians should look beyond simple reports and request specific measurements, such as the optic nerve sheath diameter and the Bern Score, to build an evidence-based case. Find the episode transcript here. Want more Dr. Andrew Callen? https://x.com/AndrewCallenMD Go to AirDoctorPro.com and use promo code BENDY_ to get UP TO $300 off today! Want to learn more about the UVA EDS Center? For Appointments and Questions: RUVAEDSCenter@uvahealth.org UVA EDS: https://www.uvahealth.com/healthy-practice/advancing-care-through-ehlers-danlos-clinic UVA EDS FAQ: https://www.uvahealth.com/support/eds/faq UVA Pediatric Integrative Medicine: https://childrens.uvahealth.com/specialties/integrative-health Want more Dr. Linda Bluestein, MD? Website: https://www.hypermobilitymd.com/ YouTube: https://www.youtube.com/@bendybodiespodcast Instagram: https://www.instagram.com/hypermobilitymd/ Facebook: https://www.facebook.com/BendyBodiesPodcast X: https://twitter.com/BluesteinLinda LinkedIn: https://www.linkedin.com/in/hypermobilitymd/ Newsletter: https://hypermobilitymd.substack.com/ Shop my Amazon store https://www.amazon.com/shop/hypermobilitymd Dr. Bluestein's Recommended Herbs, Supplements and Care Necessities: https://us.fullscript.com/welcome/hypermobilitymd/store-start Thank YOU so much for tuning in. We hope you found this episode informative, inspiring, useful, validating, and enjoyable. Join us on the next episode for YOUR time to level up your knowledge about hypermobility disorders and the people who have them. Join YOUR Bendy Bodies community at https://www.bendybodiespodcast.com/. YOUR bendy body is our highest priority! Learn more about Human Content at http://www.human-content.com Podcast Advertising/Business Inquiries: sales@human-content.com Part of the Human Content Podcast Network FTC: This video is not sponsored. Links are commissionable, meaning I may earn commission from purchases made through links Learn more about your ad choices. Visit megaphone.fm/adchoices
Galen Clavio previews the Little 500 races from Bill Armstrong Stadium as Bloomington gears up for the biggest weekend of the year — including the 75th running of the men's race. Galen is joined by two senior IU student broadcasters who will be on the call this weekend: Zach Browning (women's race play-by-play) and Nick Rodecap (men's race play-by-play). Zach breaks down the women's field, starting with Theta on the pole and the chase group behind them (including Teter, Alpha Chi Omega, Delta Gamma, Melanzana, CSF, and more), plus how weather could affect race-day strategy. Then Nick previews a loaded men's race, headlined by Cutters' dominant spring series and Black Key Bulls' quest for a three-peat — with SAE, Fiji, Sig Ep, and a deep group of contenders ready to make it a chess match over 200 laps.
Spinal cerebral spinal fluid (CSF) leaks are significantly more common in those with connective tissue disorders than many realize, yet patients often suffer for years before finding the right diagnosis. In this episode, neuroradiologist Dr. Andrew Callen joins Dr. Linda Bluestein and co-host Dr. Knight to discuss the complexities of CSF dynamics and the challenges of diagnosing leaks when routine imaging appears normal. Dr. Callen explains the different types of leaks, including the elusive CSF-venous fistula, and why common clinical assumptions, like the requirement of a low opening pressure, are often incorrect. From the Bern Score to the critical differences between Chiari malformations and positional brain sag, this conversation provides an essential roadmap for patients and clinicians navigating the "unseen" world of intracranial hypotension. Takeaways: Cerebral Spinal Fluid Basics: CSF is a clear fluid that cushions the brain and spine and plays a vital role in metabolic function. Three Major Leak Types: Leaks can occur via bone spurs poking the dura, nerve root tears (common in EDS), or CSF-venous fistulas where fluid drains into the bloodstream. Atypical Presentation: While "orthostatic headaches" (worse when upright) are classic, many patients experience vestibular symptoms like ringing in the ears, muffled hearing, imbalance, or cognitive "brain fog". The Pressure Myth: The vast majority of proven CSF leak patients do not have low opening pressure; it is a disease of low volume, not necessarily low pressure. Chiari Misdiagnosis: Positional "brain sag" can look identical to a Chiari malformation on imaging, leading to inappropriate surgical treatments if not carefully evaluated. The Bern Score: This probabilistic scoring system based on MRI findings helps radiologists determine how likely it is that a myelogram will successfully find a patient's leak. Imaging Strategy: Clinicians should look beyond simple reports and request specific measurements, such as the optic nerve sheath diameter and the Bern Score, to build an evidence-based case. Find the episode transcript here. Want more Dr. Andrew Callen? https://x.com/AndrewCallenMD Go to AirDoctorPro.com and use promo code BENDY_ to get UP TO $300 off today! Want to learn more about the UVA EDS Center? For Appointments and Questions: RUVAEDSCenter@uvahealth.org UVA EDS: https://www.uvahealth.com/healthy-practice/advancing-care-through-ehlers-danlos-clinic UVA EDS FAQ: https://www.uvahealth.com/support/eds/faq UVA Pediatric Integrative Medicine: https://childrens.uvahealth.com/specialties/integrative-health Want more Dr. Linda Bluestein, MD? Website: https://www.hypermobilitymd.com/ YouTube: https://www.youtube.com/@bendybodiespodcast Instagram: https://www.instagram.com/hypermobilitymd/ Facebook: https://www.facebook.com/BendyBodiesPodcast X: https://twitter.com/BluesteinLinda LinkedIn: https://www.linkedin.com/in/hypermobilitymd/ Newsletter: https://hypermobilitymd.substack.com/ Shop my Amazon store https://www.amazon.com/shop/hypermobilitymd Dr. Bluestein's Recommended Herbs, Supplements and Care Necessities: https://us.fullscript.com/welcome/hypermobilitymd/store-start Thank YOU so much for tuning in. We hope you found this episode informative, inspiring, useful, validating, and enjoyable. Join us on the next episode for YOUR time to level up your knowledge about hypermobility disorders and the people who have them. Join YOUR Bendy Bodies community at https://www.bendybodiespodcast.com/. YOUR bendy body is our highest priority! Learn more about Human Content at http://www.human-content.com Podcast Advertising/Business Inquiries: sales@human-content.com Part of the Human Content Podcast Network FTC: This video is not sponsored. Links are commissionable, meaning I may earn commission from purchases made through links Learn more about your ad choices. Visit megaphone.fm/adchoices
Familiarity with the clinical, MRI, CSF, and serologic features of MOGAD can help neurologists recognize this condition in clinical practice. Awareness of the utility and pitfalls of the MOG antibody test is critical. The current therapeutic approach is guided by retrospective studies and the application of immunotherapies used in other autoimmune neurologic disorders. In this episode, Gordon Smith, MD, FAAN, speaks with Eoin P. Flanagan, MBBCh, coauthor of the article "Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Flanagan is a professor of neurology and the division chair of the Division of Multiple Sclerosis and Autoimmune Neurology in the Department of Neurology at Mayo Clinic in Rochester, Minnesota. Additional Resources Read the article: Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: So, what neurological disorder can cause bilateral optic neuritis, transverse myelitis, ADEM, or can mimic acute flaccid myelitis, intracranial hypertension, viral encephalitis, or cause seizures? Sounds like the great imitator, perhaps. If you want to know and learn more about this syndrome and how you can treat it---and it is very treatable---keep listening. My name is Gordon Smith, and today I have the great opportunity to talk with Dr Eoin Flanagan from the Mayo Clinic on his article on myelin oligodendrocyte glycoprotein antibody associated disease, or MOGAD, which is in the April 2026 issue of Continuum on Multiple Sclerosis and Related Disorders. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today I'm interviewing Dr Eoin Flanagan about his article on myelin oligodendrocyte glycoprotein associated disease, or MOGAD, which appears in the April 2026 Continuum issue on multiple sclerosis and related disorders. Eoin, welcome to the podcast, and please introduce yourself to our audience. Dr Flanagan: Yeah, thanks so much. I'm Eoin Flanagan. I'm a neurologist at the Mayo Clinic. I'm originally from Ireland. I work in the neuroimmunology lab at the Mayo Clinic, and work and see patients with MS, MOG, and autoimmune disorders here in Rochester, Minnesota. Dr Smith: Your article is super interesting, I think, and this has been a really rapidly evolving area over the last, you know, many years. We have many more antibodies, and MOG is something that's been around for a while, but we've certainly learned a lot more about it. This is a topic that I think will be familiar to most of our listeners, but I wonder if maybe you can just begin by laying the foundation. Like, what is MOG? What's its typical presentation? Dr Flanagan: So, MOG is a protein on the surface of the oligodendrocyte or its CNS myelin, and it was always of interest as a potential antibody target, and initially it was investigated in multiple sclerosis. But subsequently, we recognized that the antibodies to MOG have a specific syndrome, of which about a quarter of patients are pediatric and then the remainder are adults. And they can present with a variety of syndromes, probably most commonly optic neuritis, but also acute disseminated encephalomyelitis, or ADEM. Transverse myelitis can also occur, and then some other unusual brain and brainstem cerebellar syndromes can also occur. Dr Smith: I was really impressed in the very broad phenotypic spectrum of MOG. We'll talk more about that, of course. But I wonder if maybe you can tell us when we should be ordering MOG antibody? Given this broad variability, does anyone who has a CNS demyelinating disease need a MOG assay, only specific phenotypes? What guidance do you have for our listeners? Dr Flanagan: Yeah. It's a great question. So, I think you have to be a little bit careful because the MOG antibody test is a little bit sticky. So sometimes we can see some low-positive false positives. So, we don't wanna order it in every single patient with classical MS. So, I suppose we'll start with who not to order it in. I think it's also a very optic nerve- and optic neuritis-central disease, so I think you really need to be considering this in a patient with optic neuritis who does not have lesions in the brain suggestive of multiple sclerosis. And then we think about some of the features: if the lesion, the enhancement along the optic nerve is long, if it's bilateral, if there's a lot of optic disc edema accompanying that, we tend to think about MOG antibodies. And then children with demyelinating disease, MOG is over-represented in that cohort, so it accounts for about a third of those. So, if you have a child with CNS demyelinating disease, particularly if they're under twelve, with ADEM presentations or other presentations, you probably want to be ordering the MOG antibody test. And then a longitudinally extensive transverse myelitis in adults, certain types of cerebral phenotypes that we can get into, you would want to consider ordering MOG antibodies too. Dr Smith: Now, you point out in the article that it's really important that laboratories use the cell-based assay for MOG as opposed to an ELISA, for instance. Is this something folks need to be very attentive to, or are all of the commercial laboratories now using a cell-based assay? Dr Flanagan: Yeah. I think all of the commercial labs are using cell-based assays, so we don't really get into much of an issue. There are some differences between serum and CSF, so really, serum is the optimal sample to order. There is also some differences between the live cell-based assay and the fixed cell-based assay, where the live cell-based assay may have some advantages in terms of sensitivity. And then CSF is kind of still under evaluation about its role in the condition. So in general, it's a serum test. And then we have to remember that the antibody tends to be highest at the onset, and then it goes down over time. So, if you delay your testing or you're testing a patient long after the condition, it can go negative, for example. So it tends to be highest both around the relapses and particularly at the onset of the condition. Dr Smith: You mentioned earlier that the test is sticky, which I take to mean that there is some risk for low-titer false positives. How do you navigate that situation? When should we be suspicious about a false positive? Dr Flanagan: Yeah. I think there's some very useful features that can help you. You know, the main differential diagnosis is going to be multiple sclerosis, particularly in the US, in regions of the northern US where MS is particularly common. So, you really wanna be making sure that if you get a positive result, low positive, that it's not multiple sclerosis. And some of the best discriminating features are CSF oligoclonal bands. They're about 85% in MS and about 15% in MOG, so an easy number to remember, 85 and 15. And then the lesions in MOG, the brain lesions, tend to disappear over time. So, if you have the advantage of that follow-up MRI a year down the line, about 70% of lesions in MOGAD will resolve, while in MS, as we know, the term means multiple scars, so the MS lesions tend to persist over time. So, they are two quite useful features that can help discriminate. Dr Smith: And how about specific phenotypes or areas of involvement or imaging abnormalities that suggest MOG? One of the things I found really interesting in your article is there are a host of different syndromes that I think had largely been previously described, many of them, that became clear later that these were really tied to MOG antibodies. Presumably, that's helpful in interpreting the antibody assay in that patients who have, perhaps, a borderline low titer, for instance, but have a very typical phenotype are more likely to have MOG than those who have a more clearly MS-type phenotype. Dr Flanagan: Yeah, absolutely right. Yes. So, there's certain phenotypes that we don't tend to see with MS. The acute disseminated encephalomyelitis, or ADEM, is one that's particularly common in children. And about half of people that have ADEM will be positive for the MOG antibody. So that's a syndrome you need to look out for, which would be often in children, encephalopathy, and they would have multifocal white matter lesions, sometimes involving the gray matter. A second syndrome that was an interesting discovery from a Japanese group was this unilateral cerebral cortical encephalitis, where patients can have this swelling and T2 hyperintensity, often just on one side of the brain. And it's in the cortex, and some of those patients won't have any white matter lesions. And in that situation, it's important to order the MOG antibody, and that seems to be a specific phenotype of MOGAD. But sometimes people don't think about it because the white matter is not involved. So, if you see these patients, they often present with seizures, sometimes they even have fever accompanied by it. And if you see those patients and see this radiological feature, then you really want to consider ordering the MOG antibody too. Dr Smith: Yeah, I found that really interesting. And I- actually, my next question is perhaps a good follow-up on that, is, what are the diagnostic pitfalls? You give a lot of examples of situations and I think some cases where it's easy to get tripped up and misdiagnose someone who has MOG with another fairly common neurological problem. Dr Flanagan: Yeah, I think some of the things that can help you when you're determining if the MOG is a true positive or false positive is the level of the antibodies. The super high titers, if it's a clear positive or very strong positive, the likelihood is that that is much more likely to be MOGAD than those low positives just above the cutoff. So that can be useful to help you discriminate from false positives. Those lesions, again, if all the lesions persist over time, that's going to be more suggestive of multiple sclerosis. Other diagnostic pitfalls, I suppose, if it's a syndrome that's not really associated with MOG, like peripheral neuropathy or other syndromes where we'll see some case reports, but usually I would be very cautious about those kind of presentations. So usually, having the antibody at a high level, and then also if they've had other symptoms suggestive of MOGAD, like if a patient has had recurrent optic neuritis and then they have an unusual brain syndrome, or they start out with an unusual brain syndrome and then have recurrent optic neuritis. You know, there are situations that make it more likely if they're having other typical phenotypes of the MOGAD where we can kind of expand the spectrum, but we have to be careful. Dr Smith: I was really curious about the dynamic imaging findings. And you point this out both in terms of the resolution of imaging findings, but also in that patients who have an acute MOG syndrome often have very rapid evolution of the imaging abnormalities. I'm just curious, you know, why is that, and what do you make of it? Does it have a mechanistic implication, do you think? Dr Flanagan: I don't think we know for sure. I think there's probably a lot more happening than we see on MRIs sometimes. What sometimes can happen in about 10% of patients is the initial MRI can be normal. We don't tend to see that with multiple sclerosis or NMOSD. Then what we see is it evolving over time. So, at that time, if you do a CSF, you'll often see inflammation, but we don't see the lesions. Now, that might be because the MRI is not very good at picking up cortical involvement. That can be difficult to see in MRI. Or there could be other factors. It could be a functional effect on the MOG but without frank demyelination yet, for example. Or there could be edema that you- myelin edema that you can't see as a lesion yet on MRI. But we do see that if you repeat the MRI, sometimes it'll change a lot. So, you may go from one or two lesions on the first MRI to twenty lesions on the second MRI a week later. So, it does tend to change a lot. And then over time, those lesions also resolve. So, what I say is if it's a very suspicious situation---like a child comes in with new-onset encephalitis, has inflammatory CSF---you might wanna consider repeating that MRI down the line and seeing if it's changing. And then over time, you know, a repeat MRI a year after the onset when there's brain or spinal cord lesions can be very helpful just to make sure you're on the right track, because lots of those lesions will then disappear, and that's a very clear discriminator from multiple sclerosis. Dr Smith: Yeah, thanks. I mean, I was wondering the same thing about whether that particular feature might imply, you know, a functional abnormality as opposed to more of a structural abnormality. So probably a lot more to learn as we move forward. There are now consensus diagnostic criteria that were published a couple of years ago. I think you've already touched on kind of the general approach, but do you want to speak to those? I found your summary pretty helpful. Dr Flanagan: Yeah, I think that those criteria are quite useful. They have three main parts to them. The first part is having a characteristic clinical syndrome. So, we talked about ADEM, we talked about cerebral cortical encephalitis, transverse myelitis that's often longitudinally extensive, and optic neuritis being the main syndromes, but sometimes other brainstem or cerebellar involvement can be seen. And then the second part is having a positive MOG antibody. And then there's some caveats there. So, if you have a high positive, then you don't really need any additional supportive criteria. On the other hand, if you're low positive, to get at those sticky antibodies that make sure it's not a false positive, you need some additional supportive clinical or MRI criteria. Or if you're only positive in CSF, you need that additional criteria. You also need to be negative for the aquaporin-4 antibody, because they can overlap clinically. And some of those supportive criteria are things that we talked about a little bit earlier, longer lesions within the optic nerve, bilateral involvement, involvement of the nerve sheath or optic disc edema. This is a situation, MOG antibody disease, where your fundoscope is useful and looking in the back of the eye and seeing swelling, because we don't tend to see that quite as often. It's less common in multiple sclerosis, but we often see prominent edema in MOGAD. And then in the spinal cord, the lesions tend to be central in the cord. Sometimes they form this H sign where it's restricted to the gray matter, and they tend to be longer, sometimes involving the conus. Patients will often have neurogenic bowel or bladder. And then in the brain, deep gray involvement, those large lesions along the cortex with swelling are some of the typical features. And then the final step is exclusion of another diagnosis. Just like with any test that we do in neurology, our final step is going to be to put that into context. So that's just a normal thing that we will always do when we get a group of test results back that we don't know what it means. We have to put it into context. So, make sure it's not multiple sclerosis, everything else does not look like multiple sclerosis, and then you can be on your way to make a diagnosis. Dr Smith: Definitely encourage listeners to read your article. I guess I say that with every time I- or with everyone I talk to for Continuum Audio, but the images are really fantastic and the cases are fantastic. So, everything you've described is well-illustrated, including really nice schematic sort of diagrams that help differentiate NMO from MOG and MS. So, if you like MRI scans and good imaging frameworks, then this is the article for you. Dr Flanagan: I think that's true, and the other thing is that the imaging is quite helpful because it takes a while for that antibody to come back. We're lucky at Mayo Clinic, if you work here, it, it comes back faster for you. But for many places, that time of sending it in, so a lot of times you don't know right away. So, looking at scrutinizing that MRI can be very helpful to guide you on your way and to know what you're dealing with and how to approach both the acute treatment and plans to have potentially a steroid taper after the acute treatment and those kind of things that can help guide you in that regard. Dr Smith: Yeah. So, let's talk about treatment. You know, what's your approach to treating a patient who has an acute demyelinating syndrome related to MOG? Dr Flanagan: So similar to other things, MOG is very steroid responsive. So, we use high-dose IV methylprednisolone in adults. That would be one gram IV for five days. And then we also will sometimes use oral steroids, twelve hundred and fifty milligrams. That's a bit of a hassle because it's twenty-five fifty-milligram tablets, it doesn't come in a larger tablet version. But it's very helpful to patients because they can get started on it right away. You don't have to set up an infusion center. So, we have used those oral steroids often in people who don't have access to an infusion center, are not in the hospital. And particularly as it's often optic neuritis, some of those patients are seen in the outpatient setting, so we can get in with treatment quickly. In patients where it's more severe, it doesn't recover quickly with steroids, then we would consider escalating to plasma exchange as our second-line treatment, and there's some retrospective data that suggests that plasma exchange can be useful. That's gonna be particularly for those people who don't have that quick response to steroids, or maybe more severe phenotypes like that brain involvement with ADEM or cerebral cortical encephalitis, where those patients might be in the hospital and quite unwell. I will say, we might get on to this, that sometimes MOG can be very, very severe and even fulminant, where there can be increased intracranial pressure, and these patients can be in the ICU, and it can be life-threatening. And so, it's really important to treat those patients aggressively, and some patients have even required hemicraniectomy or additional treatment. Sometimes IL-6 blocking medications have been used in that situation. So, monitoring and treating increased intracranial pressure in those rare patients, probably 2 or 3% that have the very severe attack, is important. Dr Smith: I think one of the things I found interesting, and then I'd love to get your feedback on this, is that most patients with MOG seem to have a very readily treatable disorder that's monophasic, right? You treat them with steroids, and they do well. On the other extreme, there are these patients that have a much more malignant presentation, and there are some that sound like they benefit from prophylactic or some chronic therapy. What's your approach, right? In MS, we do serial scans to monitor, and obviously, our patients are on, you know, chronic disease-modifying therapy. How do you decide when you're going to provide some sort of prophylactic therapy? How do you monitor it? How long do you continue it? Dr Flanagan: That's a great point. We don't know for sure yet, but I think for the most part, our approach has been if the patient has a single episode, they recover well from that episode. So, if that's optic neuritis, they're back to twenty/twenty vision. They have recovered well. We don't tend to use chronic maintenance immunotherapy. Sometimes after the first attack, we'll do a little bit of a slow taper, maybe over four, six weeks. We have done longer than that. And then we won't place them on any long-term treatment, because it's about 50% of patients that may have a monophasic disease, so we don't want to treat all those people who are destined never to have another relapse. On the other hand, if a patient had a very severe episode, they're in the ICU, they're intubated, some of those patients then afterwards we will start them at least temporarily on an attack prevention medication for at least a few years to get them through. Some patients will be very fearful of future relapses in that situation. Or if they don't recover well, if they're blind in one eye after an episode and then their other eye is vulnerable, or they're left with some residual deficits neurologically from a myelitis, then we would often sometimes put those patients after the first attack. But most of the time, we're gonna wait and see if they get that second attack, and then once they have the second attack, that is when we would consider a steroid-sparing medication. But I will say that there's no proven medications. We don't have any clinical trial data available yet. So some of those patients with relapsing disease, we'll either try to enroll them in a clinical trial, or we'll use an off-label treatment to try and manage their disease based on what we've learned from neuromyelitis optica or from multiple sclerosis. A few different options seem to be better, and we can maybe get into that too. Dr Smith: Yeah, let's go there. So, what options are there? You mentioned in more fulminant disease IL-6 inhibitors, and by that I assume you mean tocilizumab, but what are the options when you want to use prophylactic therapy? Dr Flanagan: So, that tocilizumab can be beneficial in the very acute situation, in that malignant situation. But also as an attack prevention treatment, the IL-6 blockers seem to- some of the retrospective data seems to look like it works reasonably well, so we work and see if we can get that approved. Another medication that can work well is IVIG or subcutaneous immunoglobulin as a maintenance treatment, so we would sometimes give that, like, at least one gram per kilogram once a month. The benefit of that is it doesn't lower your immune system, so there's some advantages there, particularly in people who may be more prone to infections, older people. So, we'll sometimes use that. But we do get into a lot of challenges with insurance coverage, and it can be difficult to get these approved by insurance because we only have retrospective data out there. So then for some patients, if they're in a region where there's a clinical trial available, we might try to enroll them in a clinical trial. And there are some clinical trials underway now, so hopefully in the future we'll be able to have some FDA-approved medications that can have some Class 1 data that we can follow. Because it's hard when you're just following retrospective data or anecdotal reports, it's a little bit difficult to know exactly how well you're doing with your treatments. Dr Smith: Well, Eoin, I wonder if we could finish up by just looking into the future, right? I mean, it sounds like a fun patient population to take care of because you've got lots of great therapies and can have a durable impact. But sure would be nice to have more evidence-based therapies and an FDA approval. What trials are going on? What's the future look like? Dr Flanagan: Yep. So, there's some trials going on in the- a couple of worldwide trials. One is on an FCRN blocker called rozanolixizumab, which is kind of like a plasma exchange-type treatment which removes your antibodies, and it's a weekly subcutaneous treatment where adults are enrolled. And the second one is called satralizumab, which is another IL-6 blocking medication. And again, that one's given once monthly under the skin. And the trial for that also includes children down to age eighteen, so for adolescents, too, that can be an option. There are trials, I believe, in Asia for tocilizumab too, and there's one starting in Australia for rituximab. So, the good news is that we're going to have some really good data down the line for lots of different agents, and we'll be able to figure out which treatments work. And this will be really of great benefit to our patients when we get that Class 1 data to kind of guide us on what we should be using and really build on the success of some of the other conditions like neuromyelitis optica spectrum disorder, where we now have four or five approved, medications that work very well. Dr Smith: Well, Eoin, thank you. This is a great conversation. I will say that it... the topic that I was a little intimidated about. I'm a simple peripheral nerve guy, as you know. But I think moreso than any other Continuum article I've read recently, I'm, like, loaded for bear. I can't wait to go back on the inpatient service and look for some MOG patients, because your article really left me feeling kind of prepared to think through this in a clinical setting. So, thank you for the conversation, and congratulations on a really wonderful piece for Continuum. Dr Flanagan: Yeah, thanks so much. Always a great honor to be involved in the Continuum, and thanks to all the readers out there. Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
What should a neurologist do when a routine MRI for migraine reveals incidental white matter lesions that look remarkably like Multiple Sclerosis (MS), despite the patient having no neurological symptoms? The Editors' Choice paper for the April 2026 issue of Practical Neurology is a practical guide to the clinical diagnosis and management of radiologically isolated syndrome (RIS). Author Dr. Audrey Reynolds¹ joins PN podcast editor Dr. Amy Ross Russell to discuss her work on how updated diagnostic criteria and advanced imaging markers now enable a more proactive, biological approach to the disease. Their discussion highlights the importance of risk stratification - using tools like CSF analysis and spinal imaging - to identify those most likely to benefit from early intervention with disease-modifying therapies. They also examine the delicate balance between preventing future disability and avoiding misdiagnosis in this rapidly evolving area of neurology. Read the paper: Radiologically isolated syndrome: a practical guide. (1) St Vincent's University Hospital, Dublin; University College Dublin, Ireland Please subscribe to the Practical Neurology podcast on your favourite platform to get the latest episodes. If you enjoy our podcast, you can leave us a review or a comment on Apple Podcasts (https://apple.co/3vVPClm) or Spotify (https://spoti.fi/4baxjsQ). We'd love to hear your feedback on social media - @PracticalNeurol. This episode was hosted by PN's podcast editor Dr. Amy Ross Russell. Production by Amy Ross Russell and Brian O'Toole. Editing by Brian O'Toole. Thank you for listening.
The diagnosis and management of idiopathic normal pressure hydrocephalus (NPH) is evolving. However, skepticism about this diagnosis persists among neurologists based upon lack of disease specific pathology, overlap with other neurodegenerative processes, and a lack of uniform diagnostic criteria. Also, prior reports of minimal or transient improvement after treatment with an invasive procedure and lack of high-quality studies has concerned some neurologists. We are joined by 2 experts in the field of movement disorders and CSF flow – Dr. Alberto Espay and Dr. Michael Williams – to discuss advances in our understanding of idiopathic NPH, the PENS trial, and evidence still needed to convince neurologists that NPH is clinical syndrome that warrants timely evaluation and treatment. Guest(s): Dr. Alberto Espay, Professor of Neurology at the University of Cincinnati; Dr. Michael Williams, Professor Neurology and Neurological Surgery at the University of Washington Interviewer: Dr. Kara Wyant, Clinical Associate Professor of Neurology at the University of Michigan Disclosures: Dr. Espay: Consultancies & Scientific Advisory Boards Mitsubishi Tanabe Pharma America (formerly, Neuroderm), Amneal, Acorda, Abbvie, Bial, Supernus (formerly, USWorldMeds), NeuroDiagnostics, Inc (SYNAPS Dx), Intrance Medical Systems, Inc., Merz, Praxis Precision Medicines, Citrus Health, and Herantis Pharma. Dr. Williams: I am a paid consultant to Aesculap regarding devices to treat hydrocephalus Dr. Wyant: Biovie - consulting, (NEW 8/2025) ongoing, UCB Pharma - research support, ended 6/2025, PhotoPharmics - research support, ongoing
On s'entretient avec Raphaël Delamarre, représentant en épargne collective et conseiller en sécurité financière (CSF) chez Delamarre Gestion de Patrimoine inc., au sujet du régime REEI. Un régime assez niché qui pourrait vous permettre de toucher jusqu'à 90 000$ en subventions.On regarde en détail :· Qui y est admissible?· Comment s'y inscrire? · Quels sont les paramètres? Et plus!Pour calculer le REEI : c'est iciBonne écoute!
In the first part of this series, Dr. Justin Abbatemarco and Dr. Shreya Louis discuss the background and evolving terminology around circulating tumor DNA, cell‑free DNA and CSF‑based testing in neurology. Read more about this abstract on the AAN website.
Agradece a este podcast tantas horas de entretenimiento y disfruta de episodios exclusivos como éste. ¡Apóyale en iVoox! Resumen del más reciente directo de CSF. Sólo para miembros de IVOOX.Escucha este episodio completo y accede a todo el contenido exclusivo de Los podcast del Monster. Descubre antes que nadie los nuevos episodios, y participa en la comunidad exclusiva de oyentes en https://go.ivoox.com/sq/134880
In this AJNR Article Summary, Dr. George Vilanilam discusses the article, "Maximizing the Conspicuity of Cerebrospinal Fluid–Venous Fistulas on Computed Tomography Myelography: Assessment of Contrast Density and Timing Effects." Contrast density, not just timing, plays the dominant role in detecting CSF-venous fistulas, with higher subarachnoid contrast significantly improving diagnostic confidence. These findings support prioritizing contrast pooling strategies during CT myelography to enhance fistula detection in patients with spontaneous intracranial hypotension.
Dr. Mauro Zappaterra trained at Harvard Medical School, holds both an MD and a PhD, and spent years in one of the most elite research labs in the world.Then he felt something move through his spine that changed everything. This episode starts with neuroscience and ends somewhere most people aren't used to going. Right now there is a fluid bathing your brain. It pulses with every heartbeat. It clears toxins from your brain while you sleep. It guided the development of every neuron you were born with. Scientists are only beginning to understand what it does. Every major ancient tradition on earth built spiritual practices around activating this exact system. They called it the Crystal Palace. The third eye. The cave of Brahma. They mapped it thousands of years before we had MRI machines to confirm it. Dr. Zappaterra believes this system is the gateway to higher consciousness. We have the ability to activate this... all of us. Visit Center for Integrated Behavioral HealthDr. Roger McFillin / Radically Genuine WebsiteYouTube @RadicallyGenuineDr. Roger McFillin (@DrMcFillin) / XSubstack | Radically Genuine | Dr. Roger McFillinInstagram @radicallygenuineContact Radically GenuineConscious Clinician CollectivePLEASE SUPPORT OUR PARTNERS15% Off Pure Spectrum CBD (Code: RadicallyGenuine)10% off Lovetuner click here
Thank you for joining us for our 2nd Cabral HouseCall of the weekend! I'm looking forward to sharing with you some of our community's questions that have come in over the past few weeks… Sarah: Hey doc! Ive been regularly gua sha'ing my face and I noticed that my face feels 'crunchy' especially at my jawline and at my lymph nodes by my ear. It doesnt seem to be improving despite regular use, is this normal or anything to be concerned? I feel it more in my left side which I seem to get more breakouts on my cheek/jawline/neck. Thank you! Margie: I just read all your cancer information because of a recent diagnosis. I have a Naturopathic doctor in addition to conventional oncologist. I'm curious your take on Esaic tea and or soursop? I told not to take it during treatment because it's a detox and we want the targeted chemo and immunotherapy to work… this is from my ND, however, research on both suggest otherwise. I'm very curious your thoughts. Thank you! Alicja: Hello Dr.Cabral, I recently run by blood work and urine test. I have pretty good results from my blood work (except high cholesterol) but I am concern about results from my urine test. It shows I have trace amount of blood in my urine and also albumin in my urine was detected (slightly above the optimal cut-off) My urine albumin is 0.3 mg/dL What can I do about this? Does that indicate early kidney damage? (BTW test was done on day 16th of my cycle) Thank you for answering my question. I appreciate all you do. Tyler: I'm a 37 year old male and I was diagnosed with a pilocytic astrocytoma brain tumor in my hypothalamus in December 2022. It was a benign tumor the size of a large egg, and I had a 15 hour surgery to remove 90% of it. 3 years later, I still have erectile dysfunction and low libido. Why is that and what can I do to fix it? I'm on Clomid for my testosterone, which is now around 500. I was on testosterone gel for a couple months but quit because of sperm impact. I test my sodium level every other week because it was low at times after my surgeries. I have a programmable shunt to help drain CSF. I don't have morning erections. Could this be from damage during the brain surgeries? Is it hormonal-related even though I'm on Clomid? Is it psychological? Please help. I listen to your podcast daily. Trish: Hi Dr C. - hoping to get some advice on your 7-day detox. I'm in my 50's and most of my life my weight has gone up and down by 30lbs. I have a problem with binging. As I've gotten older, I've learned how to control it and my triggers. I've tried the detox 3 times and I have found that it causes me to binge. Becoming too strict it throws me for a loop. I don't do the two fasting days. I fast 20 hours. I avoid all the inflammatory foods gluten, dairy, corns, eggs & nuts as I do this on a daily basis so that isn't hard for me. Giving up berries/fruit in my smoothie & some quinoa or brown rice is what starts to create me wanting to binge. I usually eat 1 sq a day 90% cacao choc too. Any advice on making the detox beneficial without following the guidelines 100%? Hope this makes sense Thank you for tuning into this weekend's Cabral HouseCalls and be sure to check back tomorrow for our Mindset & Motivation Monday show to get your week started off right! - - - Show Notes and Resources: StephenCabral.com/3712 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!
Hosts: Don Stader, Nate Novotny, Travis Barlock, and Jeffrey Olson In this episode, we reminice about the first 1000 medical minutes presented by EMM and what the next 1000 might hold. Below are all of the episodes referenced in this episode. Please go back and give them all a listen. Segment 1- Recap and Facts 1st medical minute o April 29, 2016. Almost exactly 10 years ago. o Diverticulitis and Antibiotics by Dr. Chris Holmes 1000th Medical Minute o March 30, 2026 o Treatment of burns by Aaron Lessen o Edited by Ashley Lyons and published by Jorge Chalit Favorite sub-topics have included: o Cardiovascular topics- 150 episodes o Pharmacology- 97 episodes o Toxicology- 85 episodes o Neurology- 75 episodes The "Hunting for…" cinematic universe. -Michael Hunt o 399: Hunting for Pancreatitis o 424: Hunting for Measles o 432: Hunting for UTIs o 445: Hunting for the Endotracheal Tube o 455: Hunting for PeeCP o 460: Hunting for PE in Syncope o 487: Hunting for Epiglottitis Obsession with 1966- Chris Holmes o 120: The State of Sepsis in 1966 o 125: Old School CPR - 1966 o 138: Bromide Toxicity - 1966 o 147: GI Bleed - 1966 o 675: CHF like it's 1966 Favorite drug: naloxone/narcan (9) o 7: Heroin Overdose and OTC Narcan o 464: Narcan't? o 516: Narcan and Pulmonary Edema o 931: Naloxone in Cardiac Arrest Favorite disease state: Sepsis (13) o 22: Sepsis Sofa o 219: History of Sepsis o 244: Fever in Sepsis o 263: Early Antibiotics in Sepsis o 272: More on Temperature in Sepsis o 287: Sepsis Bundles o 544: C is for Sepsis Unhinged title combinations o 84: Hypothermia and Lightning Strike: Code Blue o 203: Wine, Milk and… Vaccines!? o 216: Roller Coasters and Kidney Stones o 299: Black Death, Lice, Math, and Pottery o 427: Cookie Dough is Delicious o 670: Operation Tat-Type o 695: Einstein and Cellophane o 777: Grass, weed and ancient Rome o 781: Foxglove, dropsy, and Salvador Dali o 959: The KLM Flight Disaster and Lessons in Healthcare Communication Most frequent contributors - Aaron Lessen- 192 - Don Stader- 84 - Jarod Scott- 83 - Peter Bakes- 53 - Samuel Killian- 45 - Dylan Luyten- 41 - Erik Verzemnieks- Dozens - Michael Hunt- 34 - Travis Barlock- 30 - Ricky Dhaliwal- 25 Top female voices o Rachael Duncan, PharmD o Rachel Beham, PharmD o Meghan Hurley o Gretchen Hinson o Suzanne Chilton o Katie Sprinkle Most listened to - 8. Podcast 835: Syncope Review - 7. Podcast 766: Truth about Tramadol - 6. Podcast 839: Causes of Pancreatitis - 5. Podcast 760: Why Fentanyl is the Worst - 4. Podcast 844: Dental Infections - 3. Podcast 846: Early Repolarization vs. Anterior STEMI - 2. Podcast 845: Hyperkalemic Cardiac Arrest - 1. Podcast 847: ECMO CPR Mini-game: who has actually seen our most rare diagnoses? o 18: Lemierre's Syndrome – Septic thrombophlebitis of the internal jugular vein after oropharyngeal infection leading to septic emboli. o 139: Locked-in Syndrome – Ventral pontine lesion causing quadriplegia and inability to speak with preserved consciousness and eye movements. o 144: Moyamoya Disease – Progressive stenosis of intracranial carotids with development of fragile collateral vessels causing strokes. o 221: Cotard Delusion (Walking Corpse Syndrome) – Psychiatric disorder where patients believe they are dead or do not exist. o 240: Pott's Puffy Tumor – Frontal bone osteomyelitis with subperiosteal abscess from sinusitis causing forehead swelling. o 277: Mucormycosis (Rhizopus) – Angioinvasive fungal infection in immunocompromised patients causing rapid tissue necrosis. o 293: Transient Global Amnesia – Sudden, transient loss of ability to form new memories that resolves within 24 hours. o 329: Hypokalemic Periodic Paralysis – Episodic muscle weakness due to intracellular potassium shifts. o 374: Iliac Artery Endofibrosis – Exercise-induced fibrosis of the iliac artery causing claudication in athletes. o 466: Subacute Sclerosing Panencephalitis (SSPE) – Progressive, fatal neurodegenerative disease from persistent measles infection. o 477: Postpolypectomy Electrocoagulation Syndrome – Transmural burn of the colon after polypectomy causing localized peritonitis without perforation. o 578: Brown-Séquard Syndrome – Hemisection of the spinal cord causing ipsilateral motor/proprioception loss and contralateral pain/temperature loss. o 697: Kounis Syndrome – Acute coronary syndrome triggered by allergic reaction causing coronary vasospasm or plaque rupture. o 973: Meningitis Retention Syndrome – Acute urinary retention due to sacral nerve dysfunction during meningitis. Segment 2- Individual Interviews Segment 3- Looking forward Segment 4- Trivia Podcast 38, what is significant about diphtheria and March 18th? o On March 18th, the Iditarod is run in Alaska to commemorate a sled dog team, led by Balto, that ran from Nome to Anchorage and back to provide children in Nome with the diphtheria anti-toxin serum. Podcast 52: Syphilis the Great Imitator. The study of Syphilis or "Syphilology" evolved into the field of what? o Dermatology Podcast 121: The Poor Man's Methadone. What is the poor man's methadone? o Imodium Podcast 136: James Lind, conducted the first clinical trial in 1747 and proved that what cure what? Hint: think vitamins. o Citrus fruits cure scurvy. Podcast #213: --- and Potatoes. What food has been shown to lower LDL? o Oats Podcast #216: Roller Coasters and Kidney Stones. A study used a model of a kidney and ureter with different sized stones and put it on ------ roller coaster in Disney World. o Thunder Mountain Podcast #261. ---- was introduced to treat ACE-inhibitor induced angioendema. but later, better-powered studies showed that it had no benefit compared to standard treatment. o Icatibant Podcast #304: ---. ---- was a formal medical diagnosis, and one that dates back to 17th century when soldiers had longing for home and melancholy with a constellation of symptoms including lethargy, sadness, disturbed sleep, heart palpitations, GI complaints, and/or skin findings for which the only cure was to return home. o Nostalgia Podcast # 351: Steakhouse Syndrome. What is steakhouse syndrome? o Impacted food bolus 2/2 esophageal stricture Podcast # 362: Giant Hogweed. What can Giant Hogweed cause. o Photosensitivity, severe blisters, and burns Podcast #398: Who is gonna fail your antibiotic plan? What vital sign abnormality at triage had the highest odds ratio for treatment failure for the treatment of cellulitis with antibiotics. o Tachypnea Podcast # 458: A Tylenol a Day Keeps the ---- Away? A recent study investigated the effect of scheduled IV acetaminophen on the incidence of ---- in post-CABG patients in the ICU o Delerium Podcast 554: Sleeping Away Alzheimer's. What is the difference between white noise and pink noise? o White noise is all the surrounding sound frequencies mixed together that your brain tunes down so you don't get distracted while you're sleeping o Pink noise, or deep soothing noises, is the accentuated bass sounds like falling rain or waves crashing your brain keys into while sleeping. o Pink noise during sleep has been shown to increase stage 4, creating more CSF washout of beta amyloid. Podcast 580: Origin of PPE. Why were rubber gloves invented? o The invention of surgical gloves are credited to surgeon William Halsted. He developed gloves because one of his assistants (and later wife), Carol Hampton, was having severe irritation due to a caustic pre-op disinfecting process. They developed the rubber glove for Hampton which garnered popularity, and by the early 20th century, half of surgeons were using rubber gloves. Podcast 587: Puppies Preventing Burnout? Puppies lower stress, what activity in that study increased stress? o Coloring, because they were denied a chance to play with a puppy Podcast 596: Weather Can be a Headache. What are the three weather events that can increase the frequency of headaches? o High temp o Low humidity o High air pollution Podcast 612: Origin of Vaccines. Guess both diseases. The potential of vaccinations was first observed in the late 1600s when Jenner observed people who had cowpox never contracted ----. Years later, Louis Pasteur inoculated chickens with ---- after his assistant accidently created the first live attenuated vaccine by creating a weakened bacteria when he left the bacteria out while he went on vacation o Smallpox, cholera Podcast 670: Operation Tat-Type. In 1951, Operation Tat-Type began tattooing adults with their ---- in an effort to prepare for ---- in the time of the Cold War and the Korean War o Blood type, rapid transfusions Podcast 695: Einstein and Cellophane. Albert Einstein had ----- as a middle-aged man. Dr. Rudolph Nissen, founder of the Nissen fundoplication, performed exploratory surgery for this pain and found a ---- - The only treatment for an AAA at that time was to----, causing a fibrotic response to prevent rupture - Einstein died 7 years after this surgery, likely from his leaking abdominal aortic aneurysm o chronic abdominal pain o AAA o wrap the vessel in cellophane Podcast 748: -----. Whale blubber, honey, home fermented foods, homemade wine (especially the wine made in prison), and improperly stored canned food can all contain the toxin o Botulism Podcast 777: Grass, Weed, and Ancient Rome. Wine and wormwood and white hellborn were used in ancient rome to treat ----. o Nausea, sea sickness Podcast 821: EKGs in Syncope. Travis suggests a mnemonic for remembering additional EKG findings to look for in syncope o WOBBLER § Wolff-Parkinson-White (WPW) § Obstructed AV node § Brugada syndrome § Bifascicular block § Left Ventricular Hypertrophy (LVH) § Epsilon waves § Repolarization abnormalities Podcast 890: Outdoor Cold Air for Croup A 2023 study, published in the Journal of Pediatrics, investigated whether a 30-minute exposure to outdoor cold air could improve mild to moderate croup symptoms before the onset of steroid effects. In what country was this study conducted. o Switzerland Podcast 925: Pediatric Tongue Entrapment. Case study of a peds patient with his/her tongue stuck in a drinking cap. What was the substance that finally set it free? o Table sugar Podcast 960: Frank's Sign - A Marker for Coronary Artery Disease. What is Frank's Sign? o Bilateral earlobe crease Thank you to all that make the EMM awesome! Hosted and editted by Jeffrey Olson MS4 | Additional editting by Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf
We've all been there: waking up with that heavy "brain fog," struggling to find words, or feeling like your mental engine is idling in the mud. For years, we chalked this up to stress or "just getting older." But recent science has revealed a fascinating "night shift" happening inside your skull—a specialized waste-clearance department called the Glymphatic System . The "Power Wash" You Didn't Know You Had Unlike the rest of your body, your brain doesn't have traditional lymphatic vessels. Instead, it uses a high-pressure "rinse" of cerebrospinal fluid (CSF) to scrub away toxic metabolic trash—specifically proteins like amyloid-beta and tau, which are the hallmarks of Alzheimer's disease . The catch? This cleaning crew only clocks in when you are in deep, slow-wave sleep . During this time, your brain cells actually shrink by up to 60%, expanding the "pipes" so fluid can rush in and sweep the day's debris away . The Hormonal "Plumbers" For women, this isn't just about sleep; it's about hormones. Estrogen ($E_2$) is a master regulator of this system, helping to degrade plaques and protect the brain from oxidative "rusting" . When estrogen drops during menopause, the "pumps" can fail, leading to that all-too-familiar brain fog . Similarly, Melatonin is the "sleep gate" that triggers this rinse . It's a potent antioxidant secreted directly into the CSF, ensuring the cleaning fluid is high-quality and effective. Where Does the Trash Go? It's a relay race. The Glymphatic system picks up the trash and hands it off to the Dural Lymphatics in the lining of your brain. From there, it drains into the deep cervical lymph nodes in your neck, enters your bloodstream, and is eventually filtered by your liver and kidneys . Yes—your brain waste is ultimately excreted in your urine and feces. How to Optimize Your Rinse Tonight The Digital Sunset: Wear amber-tinted blue-light-blocking glasses 2 hours before bed . Research shows this protects your melatonin, increasing total sleep time and quality The "Glymphatic Glide": Sleep on your side (lateral position) . Use a body pillow between your knees and arms to keep your neck "pipes" open and unkinked. Manual Drainage: A 30-second morning neck massage (sweeping from the jaw down to the collarbone) helps "prime the pump" for the waste exiting your head. The Bottom Line: You can't have a clean mind with a clogged drain. Move by day, protect your light by night, and give your brain the rinse it deserves.
In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Andrew J. Solomon, MD, FAAN, who served as the guest editor of the April 2026 Multiple Sclerosis and Related Disorders issue. They provide a preview of the issue, which publishes on April 2, 2026. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Solomon is the Division Chief of Multiple Sclerosis and a Professor in the Larner College of Medicine at the University of Vermont in Burlington, Vermont. Additional Resources Read the issue: continuum.aan.com Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Full episode transcript available here Dr Jones: It's been more than 150 years since Jean-Martin Charcot first described the disease that we now know as multiple sclerosis. Since then, the tools we have to diagnose and treat this disorder have expanded enormously. So why are the diagnostic criteria for MS. still evolving? Today we're speaking with Dr Andrew Solomon, guest editor of our latest issue of Continuum on MS and related disorders. To learn more about this question and much more. Dr Jones: This is Dr Lyell Jones, editor in chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, editor in chief of Continuum, Lifelong Learning in Neurology. Today I'm interviewing Dr Andrew Solomon, who is Continuums guest editor for our latest issue of Continuum on multiple sclerosis and related disorders. Dr Solomon is a professor of neurological sciences at the University of Vermont, where he also serves as the division chief of multiple sclerosis. Dr Solomon is an internationally recognized authority on MS, particularly on the diagnostic approach to this complex disorder. Dr Solomon, welcome. Thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Solomon: Hi, everyone. This is Andy Solomon. It's a pleasure to be here with you. And I feel honored to have helped this collaborative effort that created this important tool for trainees and clinicians in practice, the Continuum issue on multiple sclerosis and related disorders. Dr Jones: Obviously, we're grateful that you've taken us on. A lot has happened in the world of MS and other neuroinflammatory disorders in the last few years, so lots to update. But as we've done over the last few podcasts, I'm going to start off the interview today, Dr Solomon, with a trivia question. And then we'll come back at the end of the podcast and give the answer. So, the trivia question is this. There are now more than 20 drugs approved by the FDA for the treatment of MS. What was the first disease-modifying therapy approved for MS? And when was it approved? So, don't answer because I know you know the answer. But we'll come back to it at the end of the interview. And our listeners can think about that question. So, let's get right to it. As many of our listeners know, the diagnostic criteria for MS. were recently revised. And you were involved with that revision. So, you're the perfect person to ask what were the major changes in the 2024 McDonald criteria, and why did we need to update them in the first place? Dr Solomon: I'm very excited about the 2024 McDonald criteria, and it was an honor to be part of that process that resulted in that manuscript. When we revise the diagnostic criteria for MS usually it's driven by accumulating data that suggests some changes or revisions might help us diagnose patients either earlier or with more accuracy. And that's certainly the case with this criteria. There was accumulating data that suggested some particular changes were important. You know, there's a lot of expert opinion involved as well. You know, there's many experts who are involved in the collaborative decisions that go into these revisions. And some of the changes in our field also pushed some of the revisions to where maybe there's not as much evidence, but where we felt it would improve care for patients with MS. This criteria, I would argue, is probably one of the most substantial revisions in over 20 years. There's multiple changes that are potentially impactful for the diagnosis of MS. Some very important changes involve the incorporation of new paraclinical tools that we can use to assess the visual pathway, as well as, imaging tools that provide high specificity for MS that we can use to substitute or dissemination in time, for instance, as well as other tools that may allow us to diagnose patients earlier than we would have in prior criteria. There's also some opportunities with the new criteria to potentially provide access in regions where some tools are more available than others. For instance, the incorporation of Kappa Free Light Chains as a substitute for oligoclonal bands may open up opportunities in regions where expertise for oligoclonal band testing are not available. That's a very qualitative test, whereas Kappa Free Light Chain index is more quantitative, less expensive and may allow CSF testing to be performed to aid the diagnosis of MS in some regions where it wasn't available previously. This criteria provides multiple pathways to the diagnosis of MS, many more than we've had in prior criteria. So, it's important to emphasize that while there's all these new tools and changes that have been incorporated, not every pathway needs to be available where you practice. What it incorporates as flexibility. It is a bit more complex looking at all of these different possibilities, but the point is this flexibility allows clinicians or providers to diagnose MS early with high accuracy based on the tools they have available. Dr Jones: I think it will be a learning curve, right? I think any time we make a change in how clinicians get accustomed to approaching a diagnosis of a disorder, it will take some time for folks to incorporate it. And I see what you mean about the complexity, but I think that's a really great point, that emphasizing the different pathways to the diagnosis is really a strength of the revision, right? Dr Solomon: I agree, I think, you know, in other disorders, particularly if you think about rheumatologic disorders, systemic rheumatologic disorders or inflammatory disorders, where over time we've not had very highly specific and sensitive biomarkers. And we've incorporated a variety of clinical and prior clinical findings, testing, laboratory testing and biopsy and other things to confirm a diagnosis. These approaches to these disorders are sort of a checklist. And I think that clinicians became familiar with that approach and were able to make diagnoses accurately this way. And I think of the new criteria in a similar way. It's not quite amenable to a checklist, but the pathways are sort of simplified with multiple options. Hopefully, using the figures, clinicians can look at the paper and see what tools they have available to help them confirm a diagnosis of MS. I think it's really important to emphasize that the diagnostic criteria for MS still does not discriminate MS from other disorders. Everyone who's listening here, you do, the clinicians do. So, to enter the diagnostic criteria and these pathways, we first have to feel confident that the patient has a clinical presentation and an MRI presentation or MRI findings that are highly suggestive of MS. That aspect of the criteria hasn't changed since, the Schumacher criteria in the 1960s. This concept of no better explanation. So, we still need to know what's typical for MS. And we need to know what signs or symptoms or findings are that might suggest another disorder, because the criteria are really only validated and tested in patients who have these presentations to start with that are typical for MS. A major change in this particular criteria is that we can now diagnose patients who are asymptomatic. Previously just called radiological isolated syndrome. Not every patient with an MRI finding concerning for MS and now being diagnosed with MS. There's other features that, must be present, but even more than before, knowing what the typical appearance of MRI lesions suggestive of MS, it is even more critical now than it was before, because in those patients who have either no symptoms or a nonspecific presentation, if we have an MRI that's highly convincing for MS and some other prior clinical findings, we can make the diagnosis. But we first need to know with some confidence what that MRI should look like. Dr Jones: So, there is a little circularity when we do these diagnostic criteria. I think our listeners who see patients will be reassured that the clinician is still in the loop. We haven't been automated out of the process yet. Dr Solomon: We need a highly sensitive and specific biomarker or a set of biomarkers for MS. We're getting closer with some of these advanced imaging findings like central vein sign and paramagnetic rim lesions. But not every patient can be diagnosed with those. And they're not required for the diagnostic criteria. In lieu of a highly sensitive and specific test. Our clinical acumen, for what we find a neurologic exam. And what we see on imaging in particular, is quite critical for ensuring that the criteria perform as well as we hope they will. Dr Jones: So, you've had the opportunity, the vantage point, to review all of these articles covering a wide variety of topics, MS, other neuroinflammatory disorders like aquaporin‑4–positive neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease, MOGAD. Anything that surprised you in these articles as you were reading through them? Dr Solomon: I think maybe for listeners, what may be surprising to some of them is that despite guidelines surrounding the use of some of our disease modifying therapies in pregnancy and breastfeeding that are published by regulatory authorities in the United States or Europe or other places, we are making other decisions for patients based on the data we have, the best data we have. Thinking about family planning is really important for us with patients who are newly diagnosed with MS, as well as through the course of their disease. This is a conversation we should be having shortly after diagnosis, because there are strategies we can take to minimize the risk of exposure of DMT around conception and to make plans for how we're going to think about DMT surrounding breastfeeding, to ensure the health of mom and the baby, and reduce risks as much as we can with the knowledge we have. I think in medicine it's quite common for us to use medications off label, right? I mean, so medications are often FDA approved for one indication. And in neurology, for instance, we find a lot of medications after their approval were quite effective for migraine prophylaxis for instance. Right? And so, it's not unusual for us to prescribe medications beyond the label. And I'm not suggesting that we necessarily ignore the advice of our regulatory authorities. But sometimes the data is accumulating really fast around some of these therapies after they're approved. Sometimes we can look towards experts and how we can navigate pregnancy and breastfeeding in MS. Dr Jones: I think that's a great point about the importance of family planning and having to use judgment. I do want to highlight to our listeners and our subscribers a fantastic article in the issue on family planning and MS and other neuroinflammatory disorders. This was written by Dr Ruth Dobson and Dr Kersten Hellwig, and I think it covers a lot of that gray area where we have to use our clinical judgment to manage these diseases in the absence of a regulatory approval. And I think, again, that's an important gap that the issue fills. And really, that's just a wonderfully written article that I think is a must-read. So, we cover lots of topics in this issue. And one of them is again a relatively newly characterized disorder, MOGAD. What's the latest in the world of MOGAD, what should our listeners be aware of? Dr Solomon: I agree, I think we're in an exciting time in CNS inflammatory disease. And this is a recently described disorder. You know, and the diagnostic criteria now is only a few years old. So, I think importantly, readers should be aware of the diagnostic criteria. This is something that, really will help us distinguish this disorder from NO spectrum disorder and MS. There's a key overlap between the MS diagnostic criteria and MOGAD. Two decades ago we saw a pediatric MS included somewhat atypical presentations like bilateral optic neuritis or acute disseminated encephalomyelitis. And we had caveats in our approaches to pediatric presentations of presumed MS, suggesting that there could be something very different than adult MS. Subsequently, we've realized that pediatric MS presents quite similarly to adult MS in terms of its clinical syndromes and MRI appearance, and many of those pediatric patients who had initially been diagnosed with MS and MOGAD. MOGAD is actually probably more common demyelinating syndrome in patients who are under 12 years old. So, the MS diagnostic criteria requires testing for MOG-IgG with a good assay, a cell-based assay, any patient being evaluated under the age of 12 or with a demyelinating syndrome to avoid misdiagnosis. Dr Jones: Thanks for that. Obviously, MOGAD is one of several disorders that have been more recently characterized and, something that our readers need to be familiar with, and there's plenty of updates within the issue on that and other topics. Okay. So now back to our Continuum audio trivia question. And just to remind our listeners, there are now more than 20 drugs approved by the FDA for the treatment of MS. What was the first disease-modifying therapy approved for MS? And when was it approved? Dr Solomon, do you want to take the honors and answer the question? Dr Solomon: Sure. It was way back in 1993. You had to get on a wait list, I believe, initially to get on it. There was some sort of lottery, and it was Betaseron. Dr Jones: Betaseron in 1993, was the first disease-modifying therapy approved by the FDA for the treatment of MS. It just shows how much water under the bridge we've had since then. 1993 was also the first year of the Jurassic Park series of movies. It was the biggest movie of the year, the song of the year in 1993 was "I Will Always Love You" by Whitney Houston. It was also the year you can tell that I look back into 1993 to see what else happened. It was also the first year the World Wide Web became publicly available, which is it kind of puts brackets on the era or the epoch of MS disease modifying therapy. And finally, the Super Bowl champs that year were the Dallas Cowboys, who unfortunately, have not had much luck in Super Bowls since the 1990s. Maybe they will have more opportunities like we've seen with MS therapeutics. So, Dr Solomon, I want to thank you for joining us today. I want to thank you for such a wonderful discussion of the latest in MS. I think the updated diagnostic criteria are really going to be critical for our listeners to understand and incorporate into their practice. Really grateful for your leadership of the issue, putting together a really stellar group of experts for all of our articles and grateful for your time today. Thank you for joining us. Dr Solomon: Thanks so much for having me. Thank all the other listeners out there for joining us as well. I'm really excited about this issue of Continuum. Dr Jones: Again, we've been speaking with Dr Andrew Solomon, guest editor of Continuums most recent issue on multiple sclerosis and related disorders. Please check it out. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the Journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. Thank you for listening to Continuum Audio.
In this SRNA “Ask the Expert” episode, Krissy Dilger of SRNA spoke with neuroimmunologist Dr. Shailee Shah about paraneoplastic neurologic syndromes—immune-mediated, “off-target” effects of cancer that can affect the brain, spinal cord, or peripheral nerves. Dr. Shah described updated diagnostic criteria and scoring that combine neurologic phenotypes, cancer risk, and high-risk autoantibodies, and she explained how immune checkpoint inhibitors can trigger immune-related neurologic adverse events that don't always fit classic rules [00:01:48]. She reviewed how these syndromes differ from other autoimmune neurologic disorders and outlined common subacute presentations such as limbic encephalitis, brainstem encephalitis, cerebellar ataxia, seizures, and neuropathies [00:08:09]. Dr. Shah emphasized prompt evaluation with neurologic exam, MRI/EEG/EMG as appropriate, blood and CSF antibody testing, cancer screening, and coordinated oncologic and immunosuppressive treatment to prevent worsening disability [00:17:24].Shailee Shah, MD is a Clinical Assistant Professor in the Neuroimmunology Division with Northwestern Medicine and Northwestern University. She is an autoimmune neurologist with expertise in the management of paraneoplastic and autoimmune neurological diseases. She also treats rare neuroimmunological diseases such as neuromyelitis optica and MOG associated disease. She is co-director of the Northwestern Medicine Paraneoplastic Neurological Disease Clinic.00:00 Welcome and Guest Intro00:58 What Is Paraneoplastic01:48 New Criteria and Antibodies04:59 Diagnostic Challenges and ICI08:09 Paraneoplastic vs Autoimmune10:22 How Common Are They13:03 Early Symptoms to Watch17:24 When to Seek Care19:09 Testing and Workup24:20 Paraneoplastic Myelitis27:55 Delays and Specialty Centers31:38 Cancer Link and Treatment37:16 Changing Therapies38:19 Recovery and Prognosis39:58 Patient Advice and Hope42:52 Closing
What are the most important steps to take after the primary survey to avoid missed injuries and set facial fractures up for a safer repair? In this episode of Everyday Oral Surgery, Dr. Andrew Jenzer returns to break down practical trauma fundamentals for oral and maxillofacial surgeons. He explores the steps for secondary surveys, core fracture repair principles, evaluating facial trauma, and making surgical decisions under pressure. He explains haemorrhagic shock staging, the Glasgow Coma Scale, cervical spine considerations, and a systematic approach for assessing trauma. He discusses the distinction between rigid and semi-rigid fixation, load-bearing versus load-sharing constructs, and how locking screws can help reduce complications. He unpacks the red flags to look out for, like orbital compartment syndrome, muscle entrapment with the oculocardiac reflex, and CSF leaks. Dr. Jenzer also shares planning guidance to help prevent missed injuries and unpacks why thin-slice CT scan reformats are vital. Tune in now!Key Points From This Episode:The four classes of hemorrhagic shock and the vital signs associated with each stage.Learn about the Glasgow Coma Scale and why a low score is a cause for concern.Understand penetrating neck trauma zones and why the zone determines the approach.Discover the difference between rigid fixation and semi-rigid fixation for fractures.Unpack the ‘ideal lines of osteosynthesis' concept and the biomechanical advantage it offers.Find out how load-bearing fixation differs from load-sharing fixation for plates and screws.Locking screws versus non-locking screws, and when is the best time to use each. Hear about the Advanced Trauma Life Support (ATLS) process and why it is important. How to confirm cervical spine safety using NEXUS criteria before proceeding.Dr. Jenzer shares his top-down, systematic approach to assessing trauma.Examples of when existing injuries have been overlooked and why.Ways to spot orbital compartment syndrome and why vision loss can be a bad sign.What muscle entrapment and the oculocardiac reflex indicate, and how to navigate it.Why thin-slice CT scans should be requested over standard thicker cuts. Explore why early airway and feeding strategies are vital to consider early on. Links Mentioned in Today's Episode:Dr. Andrew Jenzer — https://surgery.duke.edu/profile/andrew-clark-jenzer Dr. Andrew Jenzer Email Address — andrew.jenzer@gmail.com ACOMS — https://www.acoms.org/Everyday Oral Surgery Website — https://www.everydayoralsurgery.com/ Everyday Oral Surgery on Instagram — https://www.instagram.com/everydayoralsurgery/ Everyday Oral Surgery on Facebook — https://www.facebook.com/EverydayOralSurgery/Dr. Grant Stucki Email — grantstucki@gmail.comDr. Grant Stucki Phone — 720-441-6059
In this episode of the Neuroveda Podcast for Complex Health, Gillian Ehrlich, family nurse practitioner certified in Ayurveda and functional medicine, welcomes one of Neuroveda Health's own clinicians, Brianna Cardenas, DMSc, PA-C, ATC, CSC1.Dr. Cardenas is a specialist in Ehlers-Danlos syndrome (EDS), hypermobility spectrum disorders, and complex neurologic and immunologic comorbidities, including dysautonomia, mast cell activation syndrome, spinal CSF leaks, craniocervical instability, venous outflow disorders, tethered cord, adhesive arachnoiditis, and related pressure disorders. She sees patients at Neuroveda Health and provides remote consultations worldwide through her company, Healed and Empowered.Together, Gillian and Brianna explore one of the most complex and often misunderstood areas of connective tissue disease: how to differentiate common neurologic conditions in EDS and related connective tissue disorders. They discuss why these conditions are so often missed in conventional medicine, how connective tissue impacts the nervous system, and why patients are frequently shuffled between specialties without anyone seeing the full picture.This conversation covers the role of connective tissue, fascia, and the extracellular matrix in neurologic symptoms; how pressure disorders can show up as high pressure, low pressure, or fluctuating “spiky” patterns; why symptoms may worsen with position changes, head turning, lying flat, or being upright; the overlap between craniocervical instability, Eagle syndrome, Chiari-like presentations, CSF leaks, venous congestion, tethered cord, and arachnoiditis; why standard imaging is often inadequate for hypermobile patients; what symptom tracking can reveal; and practical ideas for diagnostic workup and imaging requests that may help patients and clinicians move closer to answers.Dr. Cardenas also shares how her own lived experience with severe chronic illness has shaped her clinical work and deepened her commitment to helping patients who so often fall through the cracks receive rigorous, compassionate, and collaborative care.In addition to her clinical work, Dr. Cardenas serves as an Assistant Professor in the MEDEX Northwest Physician Assistant Program at the University of Washington, where she teaches future physician assistants. She has lectured nationally and internationally on EDS and related comorbid conditions and is one of fewer than 100 certified fascial counterstrain practitioners worldwide.This episode is especially for patients, caregivers, and clinicians trying to make sense of symptoms that do not fit neatly into one specialty. It is an invitation to think more broadly, more collaboratively, and more compassionately about complex chronic illness.*Please note: This podcast is for educational purposes only and is not a substitute for individualized medical care. A podcast cannot replace a one-on-one medical visit, physical exam, or personalized diagnostic workup.
In episode 72 of Going anti-Viral, Dr Alan Winston joins host Dr Michael Saag to discuss a presentation he gave at the 2026 Conference on Retroviruses and Opportunistic Infections (CROI) entitled Neurodegeneration and Dementia Risk in Older Adults With HIV: Biomarkers and Epidemiology. Dr Winston is a Professor of HIV and Genitourinary Medicine at Imperial College London and Consultant Physician at St. Mary's Hospital, London. His research focuses on noninfectious comorbidities associated with HIV in the modern antiretroviral era, with a strong focus on central nervous system complications. He is the principal clinical investigator on the POPPY study, a cohort study describing the incidence and nature of comorbidities in HIV. Dr Winston and Dr Saag discuss the history and current understanding of neurodegeneration and dementia risk in older adults with HIV and review the impact of antiretroviral therapy and neuroinflammation. They review clinical assessment and screening for dementia and neurodegenerative disease including a detailed discussion of imaging techniques and cerebral spinal fluid (CSF) examination.0:00 – Introduction 1:30 – HIV and neurodegeneration4:37 – Current manifestations of CNS disease in older adults with HIV8:28 – Assessing cognitive health in older adults with HIV12:29 – Screening for dementia and neurodegenerative disease18:20 – Neuropsychometric testing, CSF examination, and management of CSF escape24:23 – Imaging techniques and future directionsResources:CROI 2026: https://www.croiconference.org/ __________________________________________________Produced by IAS-USA, Going anti–Viral is a podcast for clinicians involved in research and care in HIV, its complications, and other viral infections. This podcast is intended as a technical source of information for specialists in this field, but anyone listening will enjoy learning more about the state of modern medicine around viral infections.Going anti-Viral's host is Dr Michael Saag, a physician, prominent HIV researcher at the University of Alabama at Birmingham, and volunteer IAS–USA board member. In most episodes, Dr Saag interviews an expert in infectious diseases or emerging pandemics about their area of specialty and current developments in the field. Other episodes are drawn from the IAS–USA vast catalogue of panel discussions, Dialogues, and other audio from various meetings and conferences. Email podcast@iasusa.org to send feedback, show suggestions, or questions to be answered on a later episode.Follow Going anti-Viral on: Apple Podcasts YouTubeXFacebookInstagram...
In part one of this series, Dr. Aaron Zelikovich discusses the trial design and primary results. Show citation: Solomon T, Hooper C, Easton A, et al. Safety and efficacy of adjunct dexamethasone in adults with herpes simplex virus encephalitis in the UK (DexEnceph): a multicentre, observer-blind, randomised, phase 3, controlled trial. Lancet Neurol. 2026;25(2):136-146. doi:10.1016/S1474-4422(25)00454-5 Show transcript: Dr. Aaron Zelikovich: Welcome to today's Neurology Minute. My name is Aaron Zelikovich. I'm a neuromuscular specialist at Lenox Hill Hospital in New York City. Today, we'll discuss part one of a three-part series reviewing a recent article titled Safety and Efficacy of Adjunct Dexamethasone in Adults with Herpes Simplex Virus Encephalitis in the United Kingdom (DexEnceph) Study, a multicenter observer-blind randomized phase three control trial published in Lancet Neurology. In the first episode, we'll focus on the trial design and primary results. In part two, we'll discuss the clinical implications for patients with HSV encephalitis, and in part three, discuss the outcomes seen across the trial during and after an acute infection. Overall, the study found that adjunct dexamethasone did not improve outcomes in patients with CSF-confirmed HSV encephalitis. But importantly, it also did not worsen outcomes. Prior research that was non-randomized and retrospective of 45 patients with HSV encephalitis found that patients did not receive corticosteroids had worse outcomes. A different randomized trial looking at dexamethasone and HSV encephalitis was only able to recruit 41 patients and was stopped prematurely due to the lack of recruitment. Prior to the study, there was no clear evidence that adjunct steroids with acyclovir improved outcomes in HSV encephalitis. The Dex and phase three randomized clinical trial performed in the United Kingdom at 53 hospitals recruited patients from 2016 to 2022. They screened over 1,400 patients of which only 94, or 6%, were enrolled. Patients were randomized to either acyclovir only or acyclovir and intravenous dexamethasone. In order to be randomized, patients had to have a febrile illness with new onset seizure or new focal neurological sign or altered mental status as well as a positive HSV type one or two PCR from the CSF. The primary outcome for this study was the Wechsler Memory Scale Type Four Auditory Memory Index Score which was collected at 26 weeks. It had a range of 40, which is the worst outcome, to a range of 160 which was considered normal. 81 patients were included in the modified intention-to-treat analysis. Of the 13 patients, six were lost to follow-up, and seven withdrew consent. There were 39 patients in the dexamethasone group and 42 in the acyclovir-only group in the final analysis. The primary outcome of the Wechsler Memory Scale had similar scores in both groups. 71 in the dexamethasone group and 69 in the control group with a P value of 0.76. The safety profile was similar in both groups, and there were no additional safety signals found in the dexamethasone-treated group. At 26 weeks, there were 12 deaths from HSV encephalitis, six from each group, as well as a similar time to discharge between both cohorts. The DexEnceph clinical trial did not show any clear clinical benefit for dexamethasone with regards to clinical outcomes but also didn't show any increased safety concerns compared to only acyclovir. In part two, we will discuss the implications of this trial in patients with undifferentiated encephalitis and the role that steroids play in patients that HSV encephalitis is suspected. Thank you so much, and have a wonderful day.
Third-party risk is no longer a background concern for healthcare organizations -- it is a frontline challenge. Jason Kor, Principal at HITRUST, works on the company's third-party risk management team, helping enterprises understand the security risk embedded in their supply chains. The numbers tell a stark story: according to Security Scorecard, 99% of the world's 2,000 largest companies are actively connected to a vendor that has experienced a breach in the past 18 months. And Verizon's Data Breach Investigations Report shows that the share of breaches tied to a third party has doubled year over year. HITRUST exists precisely to help organizations move from awareness to action. HITRUST will be at HIMSS 2026 in Las Vegas, March 9-12, at Booth 11307. Stop playing whack-a-mole with vendor risk -- step into the VR challenge and win prizes. For organizations already holding a HITRUST certification, the team has something else waiting: a trophy recognizing the commitment to independent, external audits and rigorous security standards. For those exploring certification for the first time, the booth is a chance to understand how HITRUST compares to alternatives like SOC 2 questionnaires -- and why scalability and risk reduction make it the stronger choice for supply chain assurance. Kor puts it plainly: the audits are time-consuming and expensive because they are effective. And at the end of the process, someone reads that report and makes real business decisions based on what it contains. Two major themes converge at this year's event: supply chain risk and AI. HITRUST has already launched an AI security assessment offering, and new CSF releases are on the horizon, including a report center feature enabling online review of assessments for anti-fraud and continuous monitoring purposes. On Tuesday, March 10, 2026, from 11:10 AM to 11:30 AM, Kor will deliver a 20-minute session titled "Understanding AI Security Risk -- The New Blind Spot in TPRM and Supply Chain Resilience." The session addresses a rapidly evolving challenge: as organizations build their own generative AI tooling -- or work with third parties that have integrated AI into their products -- questions around data sovereignty, input handling, and model provenance become critical, especially in healthcare where electronic health information is at stake. Also on the HIMSS 2026 agenda from HITRUST: Ryan Patrick, Executive Vice President of TPRM Customer Solutions, joins John P. Houston of UPMC and Chuck Christian of Franciscan Health for a Brunch Briefing titled "Building Secure, Compliant, and Resilient Healthcare Systems Together" on Tuesday, March 10, 2026, from 10:30 AM to 11:45 AM at Level 1, Casanova 505. The session offers practical strategies, frameworks, and real-world lessons for organizations looking to reduce risk, enhance protection, and advance trust in an evolving threat and regulatory landscape. This is a Brand Spotlight. A Brand Spotlight is a ~15 minute conversation designed to explore the guest, their company, and what makes their approach unique. Learn more: https://www.studioc60.com/creation#spotlight GUEST Jason Kor, Principal, HITRUSThttps://www.linkedin.com/in/securityconsultantcissp/ RESOURCES HITRUST: https://hitrustalliance.net Jason Kor Session -- Understanding AI Security Risk -- The New Blind Spot in TPRM and Supply Chain Resilience (Tuesday, March 10, 2026, 11:10 AM - 11:30 AM): https://app.himssconference.com/event/himss-2026/planning/UGxhbm5pbmdfNDMyMTMxOA== Building Secure, Compliant, and Resilient Healthcare Systems Together -- Brunch Briefing (Tuesday, March 10, 2026, 10:30 AM - 11:45 AM): https://app.himssconference.com/event/himss-2026/planning/UGxhbm5pbmdfNDMzNzQwMQ== HIMSS 2026 Global Health Conference and Exhibition: https://www.itspmagazine.com/cybersecurity-technology-society-events/himss-global-health-conference-amp-exhibition-2026 Are you interested in telling your story? ▶︎ Full Length Brand Story: https://www.studioc60.com/content-creation#full ▶︎ Brand Spotlight Story: https://www.studioc60.com/content-creation#spotlight ▶︎ Brand Highlight Story: https://www.studioc60.com/content-creation#highlight KEYWORDS Jason Kor, HITRUST, Sean Martin, brand story, brand marketing, marketing podcast, brand spotlight, third-party risk management, TPRM, supply chain risk, healthcare cybersecurity, HIMSS 2026, AI security, generative AI risk, HITRUST CSF, cybersecurity certification, data sovereignty, electronic health information, vendor risk management Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.
"I can't think about cybersecurity this week; I'm thinking about 1099s."You're not alone. Many SMBs see the NIST Cybersecurity Framework (CSF) as an overwhelming manual for government contractors, not a local shop or startup. Jen Stone sits down with Daniel Eliot, NIST's lead for small business engagement. We break down the new NIST CSF 2.0 Small Business Quick Start Guide —a "small-chunk" resource designed for under-resourced organizations to move from chaos to a structured program. In this episode:Why having "everyone" responsible means "nobody" is.How to build a "reasonable" security program while managing payroll and daily operations.Why taking security seriously helps you win bigger contracts and scale safely.The exact steps (MFA, patching, backups, and more) that even large orgs get wrong.NIST ResourcesNIST (National Institute of Standards and Technology): https://www.nist.gov/Small Business Cybersecurity Corner: https://www.nist.gov/itl/smallbusinesscyberNIST CSF 2.0 (Cybersecurity Framework): https://www.nist.gov/cyberframeworkSmall Business Quick Start Guide: https://www.nist.gov/publications/nist-cybersecurity-framework-20-small-business-quick-start-guideContact Daniel and his team: smallbizsecurity@nist.govKey Term DefinitionsThe 6 Functions: Govern, Identify, Protect, Detect, Respond, and RecoverMFA: Multi-Factor Authentication—essential for account access. Patching: Updating software to fix security "holes." MSP/MSSP: Local experts you can hire to manage IT security. Timestamps00:00 – Many hats of small business owners00:26 – Daniel Eliot and NIST's Mission02:25 – Exploring the Small Business Cybersecurity Corner03:20 – What is the NIST CSF?04:26 – The Small Business Quick Start Guide for CSF 2.006:52 – How to Identify Your Most Critical Assets09:56 – When to Seek Help: Engaging MSPs and Local Resources10:52 – Defining a "Successful" Cybersecurity Program13:21 – Essential Fundamentals: MFA, Patching, and Backups15:35 – How to Engage Directly with NIST Jen Stone (MCIS, CISSP, CISA, QSA) is a Principal Security Analyst at SecurityMetrics. With 25+ years in IT and 100+ high-level assessments, Jen specializes in making complex compliance actionable for businesses of all sizes. Outside of security, she is an aerial arts enthusiast and motorcycle rider. Request a Quote for a PCI Audit ► https://www.securitymetrics.com/pci-audit Request a Quote for a Penetration Test ► https://www.securitymetrics.com/penetration-testing Get the Guide to PCI DSS compliance ► https://www.securitymetrics.com/lp/pci/pci-guide Get FREE security and compliance training ► https://academy.securitymetrics.com/ Get in touch with SecurityMetrics' Sales Team ► https://www.securitymetrics.com/contact/lets-get-you-to-the-right-place
The March 2026 recall showcases four previously posted episodes focused on clinical issues relevant to hospital-based neurologists. The episode opens with Dr. Jennifer E. Fugate discussing PRES, focusing on clinical presentation, diagnostic criteria, neuroimaging findings, and management strategies. The episode continues with Dr. Ava Easton discussing the World Health Organization's technical brief on encephalitis. In the third episode, Dr. Matthew Ryan Woodward discusses the complexities of status epilepticus, from definition through refractory and super-refractory stages. The episode concludes with Dr. Adrian Budhram discussing common challenges neurologists face when interpreting CSF results. Podcast links: Evolving Insights into the Diagnosis, Management, and Outcomes of PRES WHO Launches Technical Brief for Encephalitis Super Refractory Status Epilepticus Diagnosis, Management, and Prognostication CSF Correction Factors for Traumatic Lumbar Puncture in Adults Article links: Posterior Reversible Encephalopathy Syndrome: Evolving Insights in Diagnosis, Management, and Outcomes WHO Launches Technical Brief for Encephalitis Super Refractory Status Epilepticus Diagnosis, Management, and Prognostication Clinical Utility of CSF Correction Factors for Traumatic Lumbar Puncture in Adults Disclosures can be found at Neurology.org.
Dr. Bishal Gyawali and Dr. Tessa Cigler share the new, comprehensive, evidence-based update of the ASCO guideline on the use of hematopoietic colony-stimulating factors in patients with cancer. They discuss recommendations on primary prophylaxis, secondary prophylaxis, and treatment of febrile neutropenia along with stem cell mobilization, efficacy, safety, duration, dosing, and administration of CSFs – including biosimilars. They highlight where it is appropriate to use a CSF, and importantly, when not to use a CSF. They touch on the significance of individual patient considerations and cost implications, and future work to refine the risk factors for the development of complications of febrile neutropenia. Read the full guideline, "White Blood Cell Growth Factors: ASCO Guideline Update" at www.asco.org/supportive-care-guidelines TRANSCRIPT This guideline, clinical tools and resources are available at www.asco.org/supportive-care-guidelines. Read the full text of the guideline and review authors' disclosures of potential conflicts of interest in the Journal of Clinical Oncology, https://ascopubs.org/doi/10.1200/JCO-25-02938 Brittany Harvey: Hello and welcome to the ASCO Guidelines podcast, one of ASCO's podcasts delivering timely information to keep you up to date on the latest changes, challenges, and advances in oncology. You can find all the shows, including this one, at asco.org/podcasts. My name is Brittany Harvey, and today I'm interviewing Dr. Bishal Gyawali from Queen's University in Kingston, Ontario, Canada, and Dr. Tessa Cigler from Weill Cornell Medicine in New York, New York, co-chairs on "White Blood Cell Growth Factors: ASCO Guideline Update." Thank you for being here today, Dr. Gyawali and Dr. Cigler. Dr. Bishal Gyawali: Thank you very much for having me. It's a pleasure. Dr. Tessa Cigler: Hi there. Nice to be here as well. Brittany Harvey: Great. And then before we discuss this guideline, I'd like to note that ASCO takes great care in the development of its guidelines and ensuring that the ASCO Conflict of Interest Policy is followed for each guideline. The disclosures of potential conflicts of interest for the guideline panel, including Dr. Cigler and Dr. Gyawali, who have joined us here today, are available online with the publication of the guideline in the Journal of Clinical Oncology, which is linked in the show notes. So then I'd like to dive into the guideline that we're here today to talk about. So first, what prompted an update to this guideline on the use of hematopoietic colony-stimulating factors in patients with cancer, and what is the scope of this updated guideline? Dr. Bishal Gyawali: The last version of the guidelines from ASCO on this topic was back in 2015, so it has been more than a decade since ASCO had a guideline on the use of G-CSF in patients with cancer receiving treatment. So it was due for an update because there has been a lot more evidence based on not necessarily new drugs, but evidence for proper timing of these agents and the duration of these agents, as well as there have been a lot of new biosimilars, and there are questions about are these biosimilars equivalent or how do we choose among these different options. One is that content of the evidence that has evolved over time in the last decade, but also I think the last time we had these guidelines, the ASCO guidelines were not incorporated to have those evidence GRADE tables. So the quality of the ASCO guidelines itself has evolved over the years, so we wanted to have a new version of the guideline that includes not only the new evidence, but also contains those evidence GRADE tables that will help to quantify the benefits. And so I think it was high time, and even more than that, the newer ASCO guidelines for any guideline, they also include considerations of cost, access, equity, and all these factors that were not included in the previous version of the guideline. So I think it's only natural that with time the guideline should also evolve. Dr. Tessa Cigler: I agree completely, and just as a framework, as we all know, neutropenia and its complications, including febrile neutropenia and infections, are still an important toxicity of many myelosuppressive chemotherapies. And these neutropenic complications do require prompt evaluation and treatment and often hospitalization, and we know that hematopoietic colony-stimulating factors, which I'm going to refer to as growth factors, can reduce the duration and severity of neutropenia and the risk of febrile neutropenia, so it remains an important topic in the practice of clinical oncology. Brittany Harvey: Absolutely. It's an important topic for both clinicians and for patients who are receiving treatment for their cancer. And as you said, there was a substantial amount of literature to review here and updating everything to be in line with the GRADE evidence rating system, so there was a lot of work that you both put into this. So then next, I'd like to review the key recommendations of this guideline by clinical question. So first, what factors did the expert panel identify that should influence the decision to administer primary prophylaxis of febrile neutropenia with a CSF? Dr. Bishal Gyawali: Yeah, so I think that constitutes one of the most important recommendations in our guidelines about primary prophylaxis with G-CSF. And this is important because not only it's about when to use it, it's also about when not to use it, as in the ASCO "Choosing Wisely" campaign has also made some recommendations about this. So our guideline recommendations are also aligned with that. So first of all, we recommend that primary prophylaxis with G-CSF is recommended when the risk of febrile neutropenia because of the chemotherapy regimen is equal to or more than 20% unless an alternative chemotherapy regimen with comparable efficacy and safety that does not need G-CSF is available. And the quality of evidence to make this recommendation is high, so we give a strong strength of recommendation for this. Having said that, even for patients where the risk of febrile neutropenia is not necessarily 20%, it's a little lower, but because of other patient-related factors, the patient is at a higher risk of complications from febrile neutropenia, such as age, comorbidities, and other factors, in such case primary prophylaxis with G-CSF should be offered. And we also make a recommendation that if G-CSF is not affordable or available, then antibiotic prophylaxis can also be offered, but the evidence quality for this is low, and the strength of recommendation is very conditional. A couple of things to highlight here would be that, I think Dr. Cigler can attest to that, we ran into lots of problems about finding the data for the evidence base to say what are the patient-related factors that actually make them at a higher risk of febrile neutropenia, you know, like how did that 20% benchmark come about? Why 20%? Or when we say even if it's less than 20%, if based on other comorbidities, if the risk is higher, we tried to dig into that evidence. For example, we're talking about our "Box 1" in the guideline, what is the evidence for each item we have included under that "Box 1"? And we tried to do a lot of search to find the evidence for that, and some of them do have strong evidence, and that will tie into our future research ideas as well. And some of them actually don't have such solid evidence too, so that was one of the reasons why we ran into lots of problems about how do we quantify whether someone is at a high risk of febrile neutropenia and where that 20% benchmark comes from. Dr. Tessa Cigler: And definitely, because there's not very clear data, our guidelines definitely leave room for physician discretion in all these situations. Brittany Harvey: Absolutely. I find that in a lot of these guidelines the key point is that there's a lot of shared decision-making with patients after talking through what risk factors they may have and what is best for them in their individual clinical scenario. So then moving on to secondary prophylaxis, what factors did the expert panel identify that should influence the decision to administer secondary prophylaxis of febrile neutropenia with a CSF? Dr. Tessa Cigler: So for patients who've already experienced a neutropenic complication from a previous cycle of chemotherapy, the question is which patients should then receive prophylactic G-CSF for subsequent cycles of chemotherapy. And without a lot of evidence again to guide us, the panel really felt strongly that secondary prophylaxis should be used when a treatment delay or when a reduced dose of chemotherapy would be thought to compromise cure rates or survival outcomes. We do note that in many situations, certainly a dose reduction or a delay would be a very reasonable alternative or an additional strategy to G-CSF administration. Dr. Bishal Gyawali: Yeah, I think it's more like if there is going to be compromise in outcomes without using G-CSF, as in if we can't maintain the dose intensity and that's going to lead to inferior outcomes, then we should. But if we can reduce the dose intensity and treatment frequency and still have the same outcomes, then I guess in simple words, we're just trying to say use it when it's absolutely needed, or you can also look into other alternatives that might not need G-CSF but you could maintain the same outcomes. Brittany Harvey: Understood. It's helpful to review those options for clinicians and showing that there's not just one way to address potential neutropenic complications for later cycles of chemotherapy. So then following those recommendations for prophylaxis, what does the expert panel recommend regarding CSFs for the treatment of febrile neutropenia? Dr. Bishal Gyawali: This is an important question because this ties strongly with the "Choosing Wisely" campaign. In other words, primary and secondary prophylaxis we talked about when CSF should be used; here we make a sort of negative recommendation in that we say when CSF should not be used, because this is where we see most overuse or overtreatment with G-CSF. So first, we say that we should not be using a CSF routinely simply because a patient has neutropenia. If they are afebrile but they only have neutropenia, we recommend against using CSF just to boost neutrophil counts; that's not a meaningful metric. Then the second recommendation we make is CSF should not be routinely used as an adjunctive treatment with antibiotic therapy for patients with fever and neutropenia. So the first one was neutropenia, no fever, don't use it. The second one is okay, there is neutropenia and fever, but the treatment for that is use of antibiotic therapy, and so in such situations routinely we should not be using G-CSF just to boost the neutrophil count. And that is tied on to the third recommendation where if the patient has fever and neutropenia but is also at a very high risk for infection-related complications or who have other prognostic factors that we think will lead to poor outcomes for the patient, then in such situations, a CSF can be used as an adjunctive treatment. But we talk about the data in the manuscript, but the data show that the most that this will do is reduce the days of hospitalization by a couple of days. It actually does not have any data that it's going to improve the mortality rates. So as of now, we use the word "may be offered," it's not "should be offered," it's "may be offered" if there are other factors that we think will make the patient at the very poor risk of mortality outcomes, and the evidence quality here therefore is low and our strength of recommendation is conditional. And we also have a box that lists those items that we think might be associated with poor prognosis for the patients, but again the data for those, are they really hard evidence? No. And that is also tied with our future research recommendation that we should study more about these factors that might lead to these poor outcomes. Dr. Tessa Cigler: And again, allowing for discretion of the treating physician. Brittany Harvey: Absolutely. It's just as important to know when not to use CSFs routinely, and those risk factor boxes that you mentioned are available in the full manuscript along with the full list of recommendations, and our listeners can refer to that; a link will be in the show notes of the episode . Dr. Tessa Cigler: Just so you know, the panel, we really discussed those criteria a lot and agonized over them and gave you our best recommendations. Brittany Harvey: Definitely, and it sounds like there was varying degrees of evidence to support a lot of those risk factors, and so it's really important that the evidence supports those, but also there was expert consensus of the panel in reviewing each of those factors individually to come up with recommendations that can be applicable for all clinicians. Dr. Bishal Gyawali: If I may add, we're proud of our panel because I think our panel is quite inclusive of people representing different specialties within cancer care, as in we had radiation oncologist, we had infectious disease expert, pharmacists, and most importantly, we also had patient partners. Brittany Harvey: Absolutely. Having a multidisciplinary panel is really important for each and every guideline. So then, this is probably relevant now, but addressing a few more specific sections addressed in the guideline, what is the role of CSFs as adjuncts to progenitor cell transplantation? Dr. Tessa Sigler: Great question, and so, as solid tumor oncologists, Dr. Gyawali and I really leaned heavily on our hematology experts within the panel. The panel decided that a CSF should be used alone after chemotherapy or in combination with a CXCR4 inhibitor to mobilize peripheral blood progenitor cells. Clearly the choice of mobilization strategy depends on the type of cancer and the type of transplantation. The panel noted that a CSF should be routinely administered after autologous stem cell transplantation to reduce the risk of severe neutropenia, and that a CSF may be administered after allogeneic stem cell transplant to reduce the duration of severe neutropenia. Again, this last recommendation has not a lot of evidence to support it, and so we kind of tempered our language that it may be administered or can be considered based on clinical judgment of the physician and the clinical status of the patient. Brittany Harvey: And that really highlights the need for a multidisciplinary panel, because as you are solid tumor oncologists, you need the hematologists to make recommendations for all sorts of patients and make sure that these guidelines are comprehensive. So then moving on to another smaller subset population, for patients receiving concomitant chemotherapy and radiation therapy, are CSFs recommended? Dr. Bishal Gyawali: I think there is very little evidence for patients who are receiving radiation therapy alone, so there is no evidence to suggest the use of CSF in patients with radiation therapy alone. The bigger question is in patients who are receiving both chemo and radiation together, chemoradiotherapy. In those patients, up until now, the classical recommendation has been to avoid G-CSF use. I think in our updated guidelines we discuss a couple newer trials that are trying to address this issue, but in the totality of evidence, we still stick with the same recommendation as before, which is CSFs are not recommended in patients receiving concomitant chemotherapy and radiation therapy, especially those involving the mediastinum because the biggest evidence of harm is for these patients. Dr. Tessa Cigler: I agree completely. Brittany Harvey: Definitely. It's important to recognize when that balance of benefits and harms leans more towards harms, and so that this should not be recommended for those patients. So there are several different CSFs that are recommended in the guideline, including biosimilars. So do the recommended CSFs differ in efficacy or safety? Dr. Tessa Cigler: So as supported by evidence, and the panel all agreed, that the various forms of CSFs, including the biosimilars, really have the same evidence for efficacy and for safety, and that the choice of agent really should depend on cost, availability, accessibility, patient convenience, and sometimes disease subtypes and treatment regimens. But, in essence, these can be used interchangeably without concern for efficacy or toxicity differences. Dr. Bishal Gyawali: I completely agree. I think in terms of efficacy outcomes, I don't think there is anything to choose between these agents. The choice between these agents would largely depend on different patient and treatment-related factors: cost, availability, affordability, feasibility. We even discuss things like where does the patient live, as in how frequently the patient can commit to the cancer center, and we also discussed things like even for the daily shots of filgrastim, patients can be taught and they can get it by themselves at home. So we discussed all these factors, but in a nutshell, the choice within these agents primarily depends not on efficacy factors, but simply based on all these other factors that are equally important but which can lead to informed decision-making about what is best for a given patient. But we mention it explicitly that the biosimilars, there is nothing to choose between them, especially the biosimilars; it's about price competition and what you can get at an affordable rate. Brittany Harvey: Understood. It's great to have many different options for patients so that there's something that can work for them based off access, cost, and all these factors that you listed. As you mentioned, it may be easier for some patients to get their treatment at home rather than in clinic, and so having different options and reviewing those with patients is very important. Dr. Bishal Gyawali: As we are having this conversation, I'm thinking that we might be a very unique guideline in that I don't think in many other settings you have this many options that you are asking about, you know, choices between equally good options and making decisions based on cost. I don't think there are any other areas in oncology where we have the privilege of making these decisions based on cost and convenience and all these factors, as well as we might be one of those guidelines where we have, as discussed before, so many recommendations about when not to do things and trying to promote judicial use of treatments. Dr. Tessa Cigler: As you might imagine, our panel discussions were very lively. Dr. Bishal Gyawali: Yes. But Dr. Cigler, do you recall any other guideline where there is so much discussion about when not to use things and how we have so many biosimilar options and we can choose the one that's most appropriate? I don't recall any other. Dr. Tessa Cigler: I agree with you. Brittany Harvey: It's certainly a unique guideline in that regard. So we'll move into the last clinical question that the expert panel addressed. But what does the expert panel recommend for the initiation, duration, dosing, and administration of CSFs? Dr. Bishal Gyawali: Yeah, I think there has been some new data in this regard that were not available in the previous guideline. For example, we have new trials testing a shorter duration of filgrastim injections compared to the standard of care. So we have some data, we call this 'de-escalation of treatment'. So we have more data supporting de-escalation of treatment. We have some data for lower dose of pegfilgrastim, we have data for lower duration of filgrastim, we have also some new data about timing of treatment, as in there has been some newer data presented about the relationship of timing of the drug and the frequency of adverse events from G-CSF such as bone pain. There is also the question about, for patients who don't live near the cancer center, can they get their pegfilgrastim shot on the day of chemo while they are in the cancer center? So all these questions that are very pragmatic and important questions, but were not answered before, we're glad that we had more evidence to talk about all these factors and give a more solid recommendation to our users of the guideline. Brittany Harvey: Definitely. And listeners can review the full list of dosing and administration recommendations in Table 2 in the guideline, and that will be linked in the show notes of the episode. So then I really want to thank you both for reviewing all of these recommendations. There's certainly a large amount of clinical questions and recommendations that you went through. I'd like to next ask, in your view, what is the importance of this updated guideline and how will it impact both clinicians and patients? Dr. Bishal Gyawali: I think the importance of this updated guideline is that, as mentioned before, we talk about newer data that have come up with regards to not just the most important two questions as in when to use it as primary prophylaxis and when to use it as secondary prophylaxis and when to use it as treatment, but also with regards to the duration and timing and dosing and multiple options and how these all factors as well as patient-related factors should be combined to make an informed decision, the most appropriate decision for the patient. And as mentioned before, we have the GRADE tables that were not in the previous version of this guideline. So I think even those users that are familiar with the 2015 guideline, I think they will find very novel content in this new updated guideline, and they will find it useful for their practice. I would encourage the readers to not only read the headlines of the box recommendations, but also read the full text of these guidelines because we have worked really hard to incorporate the latest evidence and also interpret them contextually. The discussion regarding de-escalation, patient considerations, cost implications; usually, people just skip these portions when they read a guideline. But I think these are also one of the most important paragraphs in our guideline, so they have been written with very careful thought, and I think reading the whole guideline is very much worth your time. Dr. Tessa Cigler: As you can imagine, I agree completely, having just spent several months thinking about these guidelines and all their nuances. Brittany Harvey: Certainly, this guideline is definitely a very comprehensive update, and that nuance in the manuscript is really important for clinicians to understand and read through and understand when it's appropriate to make certain decisions. So then to wrap us up, I'd like to ask, what are the outstanding questions and active research areas regarding the use of white blood cell growth factors in patients with cancer? Dr. Tessa Cigler: As you all know from clinical practice and that we've said several times already in this podcast is that the risk factors for the development of complications of febrile neutropenia are still not clearly worked out. And one of the things that is, I think, really needed in clinical practice is the development of predictive algorithms or biomarkers to really allow us to understand who might be more at risk and to allow for the clinician to be able to tailor the use of G-CSF as needed. Brittany Harvey: Yes, and so we'll look forward to future updates in this space to inform new recommendations and an updated guideline in the future. So I want to thank you both so much for your work to develop this comprehensive guideline. It was certainly a lot of effort, and thank you for your time today, Dr. Gyawali and Dr. Cigler. Dr. Tessa Cigler: Oh, my pleasure. It's nice to be here and to speak with you all. Dr. Bishal Gyawali: Yeah, it was great to speak with both of you but also through you to the audience, and we had a great time. Thank you. Brittany Harvey: And then finally, thank you to all of our listeners for tuning in to the ASCO Guidelines podcast. To read the full guideline, go to www.asco.org/supportive-care-guidelines. You can also find many of our guidelines and interactive resources in the free ASCO Guidelines app, available in the Apple App Store or the Google Play Store. If you have enjoyed what you've heard today, please rate and review the podcast and be sure to subscribe so you never miss an episode. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.
Many organizations adopt security frameworks but struggle to turn them into day-to-day operations that reduce risk without slowing delivery. This talk presents a practical operating model that pairs ISO/IEC 27001 (as the certifiable management system that runs governance, risk management, internal audit, and continual improvement) with NIST Cybersecurity Framework 2.0 (as the outcome-focused "dashboard" for aligning security priorities to business objectives and communicating posture to leaders). Attendees will see how to translate business goals into CSF 2.0 current and target profiles, convert those profiles into ISO 27001 objectives and control ownership, and design "evidence by default" workflows that reduce audit fire drills. The session will include real-world design patterns (paved roads, tiered decision rights, exception handling with expiry, and control health metrics) and highlight where assurance programs often drift into "control theater." The goal is a repeatable approach that both practitioners and researchers can critique, improve, and apply. About the speaker: Danny Vukobratovich is a Sr. IT Security Analyst at Purdue University, where he manages Purdue IT's ISO program spanning ISO/IEC 27001 (information security), ISO 9001 (quality management), and ISO/IEC 20000-1 (IT service management). He also oversees Purdue IT's business continuity and disaster recovery planning, with an emphasis on building resilient, auditable operating models that support research and administrative missions. Danny's professional focus is translating risk and governance into practical mechanisms, including clear decision rights, "evidence by design," and metrics that measure control health rather than control presence. His background includes security risk assessments, incident response, monitoring and logging, identity and access management, and standards-based audits across diverse environments. Danny holds the CISSP, ISO/IEC 27001:2022 Lead Implementer, and ITIL 4 Strategic Leader certifications, and an M.S. in Cybersecurity Management.
Hey everyone! Today we sat with Brendan the founder of Dyme PSI. Dyme has taken the boring AN fitting to a new level. Brendan listened to the community and heard the pains and issues that AN fittings has caused and offered a solution. He introduced a new and better AN fitting to the community and it took off. Moving from Australia to the US in 2008, Brendan worked for a few companies before deciding to go on his own in 2020 to start Dyme PSI. Now Dyme is working with builders in every aspect of the community from imports to top fuel drag racers. He has even teamed up with CSF, GReddy, Trust and more. It was a true pleasure to sit and talk with Brendan and I enjoyed his dry humor. I love conversations like this. Enjoy! Guest: @DymePSI Host: @Frank_Downstar Supported by: @Downstar @Downstar_Skate Downstarinc.com HyperURL.co/Downstar @DowntimeWithDownstar
Not Just a Chiropractor for Stamford, Darien, Norwalk and New Canaan
Cerebrospinal fluid (CSF) is a clear liquid that acts like a cushion for your brain and spinal cord. It also helps wash away waste and brings nutrients to your brain. Normally, this fluid flows through tunnels in your brain and down your back.Think of it like a plumbing system in a house. If a pipe gets clogged or squeezed, the water has nowhere to go and starts to build up. When the flow of CSF is blocked, the fluid builds up inside your head. This creates extra pressure against your brain and the inside of your skull, which causes a painful headache.Common reasons for this "clog" include:The shape of the skull: Sometimes the back of the skull is too small, pushing part of the brain downward and blocking the fluid's path.A "kink" in the pipe: If the neck or spine is out of alignment, it can squeeze the space where the fluid flows.Injury: A bad bump or fall can sometimes cause swelling that slows down the flow.When the pressure is relieved and the fluid can flow freely again, the headaches usually go away. That is why chiropractic care should be an obvious choice for resolving headaches.Core Health Darienlink to schedulehttps://calendly.com/corehealth/headacheThis podcast welcomes your feedback here are several ways to reach out to me. If you have a topic you would like to hear about send me a message. I appreciate your listening. Dr. Brian Mc Kayhttps://twitter.com/DarienChiro/https://www.facebook.com/ChiropractorBrianMckayhttps://chiropractor-darien-dr-brian-mckay.business.sitehttps://podcasts.apple.com/us/podcast/not-just-chiropractor-for-stamford-darien-norwalk-new/id1503674397?uo=4Core Health Darien-Dr.Brian Mc Kay 551 Post RoadDarien CT 06820203-656-363641.0833695 -73.46652073GMP+87 Darien, Connecticuthttps://youtu.be/WpA__dDF0O041.0834196 -73.46423349999999https://darienchiropractor.comhttps://darienchiropractor.com/darien/darien-ct-understanding-pain/Find us on Social Mediahttps://chiropractor-darien-dr-brian-mckay.business.site https://www.youtube.com/channel/UCNHc0Hn85Iiet56oGUpX8rwhttps://docs.google.com/spreadsheets/d/1nJ9wlvg2Tne8257paDkkIBEyIz-oZZYy/edit#gid=517721981https://goo.gl/maps/js6hGWvcwHKBGCZ88https://www.youtube.com/my_videos?o=Uhttps://www.linkedin.com/in/darienchiropractorhttps://www.facebook.com/ChiropractorBrianMckayhttps://sites.google.com/view/corehealthdarien/https://sites.google.com/view/corehealthdarien/home
We review diagnosing and managing bacterial meningitis in the ED. Hosts: Sarah Fetterolf, MD Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Meningitis_2_0.mp3 Download Leave a Comment Tags: CNS Infections, Infectious Diseases, Neurology Show Notes Core EM Modular CME Course Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. Course Highlights: Credit: 12.5 AMA PRA Category 1 Credits™ Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics. Cost: Free for NYU Learners $250 for Non-NYU Learners Click Here to Register and Begin Module 1 Patient Presentation & Workup Patient: 36-year-old male, currently shelter-domiciled, presenting with 3 weeks of generalized weakness, fevers, weight loss, and headaches. Vitals (Initial): BP 147/98, HR 150s, Temp 100.2°F, RR 18, O2 99% RA. Clinical Evolution: Initial assessment noted cachexia and a large ventral hernia. Following initial workup, the patient became acutely altered (A&O x0) and febrile to 102.9°F. Physical Exam Findings: Brudzinski Sign: Positive (knees flexed upward upon passive neck flexion). Kernig Sign: Discussed as highly specific (resistance/pain during knee extension with hip flexed at 90°). Meningeal Triad: Fever, nuchal rigidity, and AMS (present in 40% of cases; 95% of patients have at least two of the four cardinal symptoms including headache). Imaging: Chest X-ray: Scattered opacities (pneumonia) and a small pneumothorax. CT Abdomen/Pelvis: Confirmed asplenia (secondary to 2011 GSW/exploratory laparotomy). Head CT: Ventricle enlargement concerning for obstructive hydrocephalus and diffuse sulcal effacement. CSF Analysis & Microbiology Bacterial Meningitis Opening Pressure: Elevated (Normal is 1000–2000/mm3 WBC); dominated by neutrophils (>80% PMN). Glucose: Low (
Daniel Gewolb guides Jennifer Gillespie and Francis Deng through a series of skull base MRI scenarios. Includes discussion of neurovascular compression, pulsatile tinnitus, skull base osteomyelitis, CSF leak and more. Meanwhile, we learn that Frank is a naughty boy who breaks rules. Radiopaedia Lecture Collection ► https://radiopaedia.org/courses/lecture-collection Radiopaedia 2026 ► https://radiopaedia.org/courses/radiopaedia-2026-virtual-conference Become a supporter ► https://radiopaedia.org/supporters Get an All-Access Pass ► https://radiopaedia.org/courses/all-access-course-pass Radiopaedia Community chat ► http://radiopaedia.org/chat Ideas and Feedback ► podcast@radiopaedia.org The Reading Room is a radiology podcast intended primarily for radiologists, radiology registrars and residents.
Behind closed doors, lawmakers decide the future of hunting, fishing, and access to public lands. Host Fred Bird sits down with a panel of seasoned policy experts to unpack one of the most consequential issues facing hunters and anglers today: the fight over public lands and wildlife management. This isn't surface-level debate—it's a clear-eyed look at how decisions are actually made, who influences them, and why sportsmen need to pay attention long before legislation hits the headlines. Joined by CSF's Sr VP Taylor Schmitz, and Delta Waterfowl's Chief Policy Officer, John Devney and VP of Government Affairs, Cyrus Baird, the crew breaks down the recent public lands battle and explains the formal process that governs how federal lands are managed, from National Wildlife Refuges to multi-use landscapes critical for hunting access and fishing opportunity. Listeners will gain insight into the outsized role state legislators play in shaping land use policy, wildlife funding, and access for future generations of hunters, anglers, and outdoor families. Fred and his guests also explore the growing importance of caucus networks—organized groups of lawmakers and advocates working behind the scenes to protect wildlife habitat, sustain public access, and keep conservation grounded in sound science. The discussion highlights the challenges facing the National Wildlife Refuge System, including declining awareness and the real consequences that come with disengaged communities. This episode equips sportsmen with the context needed to engage intelligently, advocate effectively, and ensure America's public lands remain places where hunting, fishing, and outdoor traditions can thrive. Get the FREE Sportsmen's Voice e-publication in your inbox every Monday: www.congressionalsportsmen.org/newsletter Learn more about your ad choices. Visit megaphone.fm/adchoices
You start with Quick Tips that tighten up your daily Apple workflow fast. You learn how CarPlay scrubbing actually works while driving, how Siri can jump forward or back in precise time chunks, and why Apple's vision for Siri, Gemini, and personal intelligence matters more than the hype suggests. You unlock practical wins like copying Voice Memos transcripts, using Continuity for clipboard magic across devices, mastering iPhone copy and paste gestures, and understanding when dragging photos quietly converts them to JPEGs. Along the way, you revisit Apple Newton roots, discover why tools like Yoink still matter, and pick up slick tricks for prepping images in Messages and pausing voice recordings mid-thought. Then you move into real-world problem solving. You figure out how to record a selfie video on iPhone while reading a script without breaking your flow, why Sign in With Apple is still worth using, and how to monitor drive health without guessing. You finally get clarity on weird Trash behavior, stop your mouse from waking your Mac, and understand why green bubble RCS and SMS sometimes fail on macOS. The episode wraps with a discussion about Apple Creator Studio tools like Logic Pro, Final Cut Pro, Pixelmator Pro, Compressor, MainStage, and premium content across Apple's productivity apps. Listen to sharpen your instincts so when it counts, you Don't Get Caught. 00:00:00 Mac Geek Gab 1125 for Monday, January 19th, 2026 January 19th: Brew a Potion Day MGG Monthly Giveaway – Enter to win a copy of Ecamm Live or Carbon Copy Cloner 7! The MGG Merch Store is Live! MGG's CES 2026 Sponsors: BusyCal (with code MACGEEK10)! Eero Ecamm for Zoom integration MacPaw CCC Backup Quick Tips 00:00:01 Chris-QT-CarPlay lets you scrub while driving 00:04:01 QT-Use Siri to skip forwards and backwards in specific time increments 00:06:18 The future of Siri, Gemini, and Personal Intelligence 00:14:33 QT-See and copy transcripts from Voice Memos 00:15:44 QT-Continuity works for Clipboard Too 00:18:21 iPhone Copy/Paste Gestures 00:21:55 Doug-QT-Dragging photos on iPhone converts them to JPEG Copying/Pasting on the Apple Newton Yoink 00:27:01 Jeff-QT-Dragging an image into Messages preps it to send 00:28:15 Pete-QT-Pause Voice Recording on iOS 00:29:54 How do I record a selfie video on my iPhone while being able to read a script? Teleprompter for Video for iPhone Also Teleprompter is free with in app purchases 00:34:43 GW-QT-Don’t forget about Sign in With Apple Sponsors 00:38:50 SPONSOR: Tempo. For a limited time, Tempo is offering my listeners SIXTY PERCENT OFF your first box! Go to TempoMeals.com/MGG. 00:40:22 SPONSOR: Stamps.com. Try Stamps dot com risk-free for sixty days at stamps.com and use code mgg! Sixty days gives you plenty of time to see exactly how much time and money you’re saving on every shipment. 00:41:42 SPONSOR: CleanMyMac. Get Tidy Today! Try 7 days free and use our code MACGEEK for 20% off at clnmy.com/MACGEEK Your Questions Answered and Tips Shared! 00:43:12 Andy-What should I use to monitor drive health? Disk Drill DriveDx Techtool Pro for repairing APFS volumes 00:48:52 Gary-Why Sometime Trash? Why Sometimes NO Trash? 00:59:37 Andrew-How can I keep my mouse from waking up my Mac? 01:03:25 Caleb-Why can’t I send green bubble RCS/SMS messages from my Mac? Cool Stuff Found 01:07:19 CSF? Apple Creator Studio Logic Pro Pixelmator Pro Final Cut Pro Compressor MainStage Premium content for Pages, Numbers, Keynote, Freeform, Motion and more 01:18:31 MGG 1125 Outtro MGG Monthly Giveaway Bandwidth Provided by CacheFly MGG's CES 2026 Sponsors Pilot Pete's Aviation Podcast: So There I Was (for Aviation Enthusiasts) The Debut Film Podcast – Adam's new podcast! Dave's Business Brain (for Entrepreneurs) and Gig Gab (for Working Musicians) Podcasts MGG Merch is Available! Mac Geek Gab YouTube Page Mac Geek Gab Live Calendar This Week's MGG Premium Contributors MGG Apple Podcasts Reviews feedback@macgeekgab.com 224-888-GEEK Active MGG Sponsors and Coupon Codes List BackBeat Media Podcast Network
In the final installment of this series, Dr. Justin Abbatemarco and Dr. Divyanshu Dubey discuss the latest findings and some non-occupational exposures. Show citation: Hinson SR, Gupta P, Paramasivan NK, et al. Neural synaptic vesicle autoimmunity following aerosolized porcine neural tissue exposure: insights into autoimmune inflammatory polyradiculoneuropathy. EBioMedicine. 2025;122:106053. doi:10.1016/j.ebiom.2025.106053 Show transcript: Dr. Justin Abbatemarco: Hello, and welcome back. This is Justin Abbatemarco. I'm here with Divyanshu Dubey, discussing his article, Neural Synaptic Vesicle Autoimmunity Following Aerosolized Porcine Neural Tissue Exposure: Insights Into Autoimmune Inflammatory Polyradiculoneuropathy. Div, maybe we could talk about non-occupational exposures? I think many of us don't see this cohort of patients commonly, but I really think this helps inform care, beyond just this specific occupational exposure. What did you guys find in your work? Dr. Divyanshu Dubey: So, one of the inspirations for this study was driven by the phenotypic characterization of patients who were described in this 2010 paper, which is somewhat similar to some of the patients I currently see in my clinic who don't seem to meet GBS or CIDP criteria. But, based on their MRI findings, based on their CSF studies, the EMG nerve conduction studies, they seem to have this polyradiculoneuropathy presentation, often presenting with asymmetric disease onsets, starting on one leg and then sometimes transitioning to the other side. In some cases, even a non-length dependent pattern with sort of proximal cervical brachial nerve root plexus involvements, which don't really seem to have a blood test, or a biomarker right now. Currently, many of these cases are a diagnosis of exclusion. I was thinking if there's a biomarker that we can identify from this 2006 to 2008 unfortunate event, that might actually help us diagnose these patients. So, once we identified synaptophysin and GAP43 antibodies in the swine abattoir cohort, I went back to our storages of these patients with other inflammatory polyradiculoneuropathy, and found about 5% of these patients from a large cohort of close to 300 patients, did have these antibody biomarkers. Some of these patients had paraneoplastic trigger, where we had patients with neuroendocrine tumors, or hematological malignancies mounting a response to these antibodies. But a good chunk of these patients we did not truly understand, or know what the triggers were. That might be a potential for future studies, as we expand our cohort of these antibodies, as well as study further the phenotypic characterization of these cases. Dr. Justin Abbatemarco: Yeah, there's just so much there, really helping to inform future clinical care outside of this very specific occupational exposure. And then, as we talked about in the podcast, I think really helping to think through how neurological autoimmune diseases develop. So, just really exciting work. We really appreciate you coming on, sharing this. We're excited for how this evolves over the coming years. Dr. Divyanshu Dubey: Thank you, Justin.
What happens when offshore rigs become thriving fisheries and why lawmakers are finally paying attention. Kicking off 2026, The Sportsmen's Voice Roundup goes straight to Capitol Hill for a timely update on one of the most important fisheries conservation tools in the country: the Rigs to Reefs program. Fresh off congressional testimony, Chris Horton, CSF's Sr. Director of Fisheries Policy, breaks down what sportsmen and women need to understand about how offshore energy structures are transformed into long-term fish habitat and why that matters for coastal ecosystems and recreational fishing access. This conversation goes beyond politics and into the science. You'll hear how artificial reef structures support real fish productivity, increase biomass, and create ecosystems that simply wouldn't exist without them. Drawing on decades of data and peer-reviewed research, Horton explains why Rigs to Reefs isn't just about attraction, but about sustaining healthy saltwater fisheries for generations of anglers. The episode also tackles common misconceptions around offshore policy, including cost-sharing, industry involvement, and how state fish and wildlife agencies reinvest funds directly into fisheries management and habitat improvement. For anyone passionate about saltwater fishing, coastal conservation, or how federal and state policy shapes the outdoors we enjoy, this is an insider look at how conservation, science, and legislation intersect. Whether you're a Gulf Coast angler, a traveling sportsman, or someone who cares about the future of America's fisheries, this episode provides clarity on why these structures are worth fighting for and how the sporting community can play a role in shaping the outcome. Get the FREE Sportsmen's Voice e-publication in your inbox every Monday: www.congressionalsportsmen.org/newsletter Follow The Sportsmen's Voice wherever you get your podcasts: https://podfollow.com/1705085498 Learn more about your ad choices. Visit megaphone.fm/adchoices
In part one of this two-part series, Dr. Stacey Clardy and Drs. Ayush Gupta and Kuntal Sen discuss the key clinical features that should shift suspicion from autoimmune encephalitis or demyelinating disease to monogenic mimics. Show citation: Gupta A, Sahjwani D, Kahn I, Gombolay GY, Sen K. Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults: An Evolving Landscape. Neurol Genet. 2025;11(6):e200326. Published 2025 Nov 25. doi:10.1212/NXG.0000000000200326 Show transcript: Dr. Stacey Clardy: Hi, this is Stacey Clardy from the Salt Lake City VA in the University of Utah. For a two-part podcast series, I've been speaking with Ayush Gupta from the University of Nebraska Medical Center and Kuntal Sen from Children's National Hospital in Washington DC about the monogenic disorders that mimic neuroinflammatory disease that are lurking in all of our clinics just waiting to be diagnosed. Ayush, for the minute, when you're seeing a patient with a presumed autoimmune encephalitis or demyelinating disease, what single cluster of features should instead most strongly push us to think of monogenic mimics at the top of our differential? Dr. Ayush Gupta: So when you are seeing a patient with presumed autoimmune encephalitis or a demyelinating disorder, cluster of features such as earlier onset in terms of age, developmental delays, CSF or imaging finding that's non-concordant with the diagnosis such as a non-inflammatory CSF, a symmetric white matter or deep gray matter involvement and relentless progression despite immunotherapy, these are the red flags where you should stop, seriously consider the possibility of a monogenic disorder and reach out to help from colleagues. Dr. Stacey Clardy: That's a great list, and we get into far more detail in the two-part podcast series. So please listen to both of those and take a read of the neurology genetics review titled Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults: An Evolving Landscape.
In part one of this two-part series, Dr. Shuvro Roy explains idiopathic normal pressure hydrocephalus (iNPH), its diagnostic challenges, and a study on whether dopamine transporter (DAT) scan results affect gait improvement after a CSF tap test. Show citation: Kim M, Park YH, Song YS, et al. Gait Improvement Following CSF Tap Test in NPH Patients With and Without Striatal Dopaminergic Deficit: A Preliminary Study. Neurol Clin Pract. 2025;15(6):e200549. doi:10.1212/CPJ.0000000000200549
In our final Freedom to Learn episode of the year, Darla Romfo, President and CEO of the Children's Scholarship Fund, joins the podcast to trace the origins of the nation's most influential privately-funded school choice efforts. Darla recounts how CSF's founders, Ted Forstmann and John Walton, sparked a national movement by empowering low-income families with […]
The lymphatic system, or lymphoid system, is one of the components of the circulatory system, and it serves a critical role in both immune function and surplus extracellular fluid drainage. Components of the lymphatic system include lymph, lymphatic vessels and plexuses, lymph nodes, lymphatic cells, and a variety of lymphoid organs. The pattern and form of lymphatic channels are more variable and complex but generally parallel those of the peripheral vascular system. The lymphatic system partly functions to convey lymphatic fluid, or lymph, through a network of lymphatic channels, filter lymphatic fluid through lymph nodes and return lymphatic fluid to the bloodstream, where it is eventually eliminated. Nearly all body organs, regions, and systems have lymphatic channels to collect the various byproducts that require elimination . Liver and intestinal lymphatics produce about 80% of the volume of lymph in the body. Notable territories of the body that do not appear to contain lymphatics include the bone marrow, epidermis, as well as other tissues where blood vessels are absent. The central nervous system was long considered to be absent of lymphatic vessels until they were recently identified in the cranial meninges. Moreover, a vessel appearing to have lymphatic features was also discovered in the eye. The lymphatic system is critical in a clinical context, particularly given that it is a major route for cancer metastasis and that the inflammation of lymphatic vessels and lymph nodes is an indicator of pathology. Structure The lymphatic system includes numerous structural components, including lymphatic capillaries, afferent lymphatic vessels, lymph nodes, efferent lymphatic vessels, and various lymphoid organs. Lymphatic capillaries are tiny, thin-walled vessels that originate blindly within the extracellular space of various tissues. Lymphatic capillaries tend to be larger in diameter than blood capillaries and are interspersed among them to enhance their ability to collect interstitial fluid efficiently. They are critical in the drainage of extracellular fluid and allow this fluid to enter the closed capillaries but not exit due to their unique morphology. Lymphatic capillaries at their blind ends are composed of a thin endothelium without a basement membrane. The endothelial cells at the closed end of the capillary overlap but shift to open the capillary end when interstitial fluid pressure is greater than intra-capillary pressure. This process permits lymphocytes, interstitial fluid, bacteria, cellular debris, plasma proteins, and other cells to enter the lymphatic capillaries. Special lymphatic capillaries called lacteals exist in the small intestine to contribute to the absorption of dietary fats. Lymphatics in the liver contribute to a specialized role in transporting hepatic proteins into the bloodstream. The lymphatic capillaries of the body form large networks of channels called lymphatic plexuses and converge to form larger lymphatic vessels. Lymphatic vessels convey lymph, or lymphatic fluid, through their channels. Afferent (toward) lymphatic vessels convey unfiltered lymphatic fluid from the body tissues to the lymph nodes, and efferent (away) lymphatic vessels convey filtered lymphatic fluid from lymph nodes to subsequent lymph nodes or into the venous system. The various efferent lymphatic vessels in the body eventually converge to form two major lymphatic channels: the right lymphatic duct and the thoracic duct. The right lymphatic duct drains most of the right upper quadrant of the body, including the right upper trunk, right upper extremity, and right head and neck. The right lymphatic trunk is a visible channel in the right cervical region just anterior to the anterior scalene muscle. Its origin and termination are variable in morphology, typically forming as the convergence of the right bronchomediastinal, jugular, and subclavian trunks, extending 1 to 2 centimeters in length before returning its contents to the systemic circulation at the junction of the right internal jugular, subclavian, and/or brachiocephalic veins. The thoracic duct, also known as the left lymphatic duct or van Hoorne's canal, is the largest of the body's lymphatic channels. It drains most of the body except for the territory of the right superior thorax, head, neck, and upper extremity served by the right lymphatic duct. The thoracic duct is a thin-walled tubular vessel measuring 2 to 6 mm in diameter. The length of the duct ranges from 36 to 45 cm. The thoracic duct is highly variable in form but typically arises in the abdomen at the superior aspect of the cisterna chyli, around the level of the twelfth thoracic vertebra (T12). The cisterna chyli, from which it extends, is an expanded lymphatic sac that forms at the convergence of the intestinal and lumbar lymphatic trunks extending along the L1-L2 vertebral levels. The cisterna chyli is present in approximately 40-60% of the population, and in its absence, the intestinal and lumbar lymphatic trunks communicate directly with the thoracic duct at the T12 level. As a result, the thoracic duct receives lymphatic fluid from the lumbar lymphatic trunks and chyle, composed of lymphatic fluid and emulsified fats, from the intestinal lymphatic trunk. Initially, the thoracic duct is located just to the right of the midline and posterior to the aorta. It exits the abdomen and enters the thorax via the aortic hiatus formed by the right and left crura of the diaphragm, side by side with the aorta. The thoracic duct then ascends in the thoracic cavity just anterior and to the right of the vertebral column between the aorta and azygos vein. At about the level of the fifth thoracic vertebra (T5), the thoracic duct typically crosses to the left of the vertebral column and posterior to the esophagus. From here, it ascends vertically and usually empties its contents into the junction of the left subclavian and left internal jugular veins in the cervical region. To ensure that lymph does not flow backward, collecting lymphatic vessels and larger lymphatic vessels have one-way valves. These valves are not present in the lymphatic capillaries. These lymphatic valves permit the continued advancement of lymph through the lymphatic vessels aided by a pressure gradient created by vascular smooth muscle, skeletal muscle contraction, and respiratory movements. However, it is important to note that lymphatic vessels also communicate with the venous system through various anastomoses. Lymph nodes are small bean-shaped tissues situated along lymphatic vessels. Lymph nodes receive lymphatic fluid from afferent lymphatic vessels and convey lymph away through efferent lymphatic vessels. Lymph nodes serve as a filter and function to monitor lymphatic fluid/blood composition, drain excess tissue fluid and leaked plasma proteins, engulf pathogens, augment an immune response, and eradicate infection. Several organs in the body are considered to be lymphoid or lymphatic organs, given their role in the production of lymphocytes. These include the bone marrow, spleen, thymus, tonsils, lymph nodes, and other tissues. Lymphoid organs can be categorized as primary or secondary lymphoid organs. Primary lymphoid organs are those that produce lymphocytes, such as the bone marrow and thymus. Bone marrow is the primary site for the production of lymphocytes. The thymus is a glandular organ located anterior to the pericardium. It serves to mature and develop T cells, or thymus cell lymphocytes, in response to an inflammatory process or pathology. As individuals age, both their bone marrow and thymus reduce and accumulate fat. Secondary lymphoid organs serve as territories in which immune cells function and include the spleen, tonsils, lymph nodes, and various mucous membranes, such as in the intestines. The spleen is a purplish, fist-sized organ in the left upper abdominal quadrant that contributes to immune function by serving as a blood filter, storing lymphocytes within its white pulp, and being a site for an adaptive immune response to antigens. The lingual tonsils, palatine tonsils, and pharyngeal tonsils, or adenoids, work to prevent pathogens from entering the body. Mucous membranes in the gastrointestinal, respiratory, and genitourinary systems also function to prevent pathogens from entering the body. Lymph Lymphatic fluid, or lymph, is similar to blood plasma and tends to be watery, transparent, and yellowish in appearance. Extracellular fluid leaks out of the blood capillary walls because of pressure exerted by the heart or osmotic pressure at the cellular level. As the interstitial fluid accumulates, it is picked up by the tiny lymphatic capillaries along with other substances to form lymph. This fluid then passes through the lymphatic vessels and lymph nodes and finally enters the venous circulation. As the lymph passes through the lymph nodes, both monocytes and lymphocytes enter it. Lymph is composed primarily of interstitial fluid with variable amounts of lymphocytes, bacteria, cellular debris, plasma proteins, and other cells. In the GI tract, lymphatic fluid is called chyle and has a milk-like appearance that is chiefly due to the presence of cholesterol, glycerol, fatty acids, and other fat products. The vessels that transport the lymphatic fluid from the GI tract are known as lacteals. Embryology The development of the lymphatic system is known from both human and animal, especially mouse studies. The lymphatic vessels form after the development of blood vessels, around six weeks post-fertilization. The endothelial cells that serve as precursors to the lymphatics arise from the embryonic cardinal veins. The process by which lymphatic vessels form is similar to that of the blood vessels and produces lymphatic-venous and intra-lymphatic anastomoses, but diverse origins exist for components of lymphatic vessel formation in different regions. Six primary lymph sacs develop and are apparent about eight weeks post-fertilization. These include, from caudal to cranial, one cisterna chyli, one retroperitoneal lymph sac, two iliac lymph sacs, and two jugular lymph sacs. The jugular lymph sacs are the first to develop, initially appearing next to the jugular part of the cardinal vein. Lymphatic vessels then form adjacent to the blood vessels and connect the various lymph sacs. The lymphatic vessels primarily arise from the lymph sacs through the process of self-proliferation and polarized sprouting. Stem/progenitor cells play a huge role in forming lymphatic tissues and vessels by contributing to sustained growth and postnatally differentiating into lymphatic endothelial cells. Lymphatic channels from the developing gut connect with the retroperitoneal lymph sac and the cisterna chyli, situated just posteriorly. The lymphatic channels of the lower extremities and inferior trunk communicate with the iliac lymph sacs. Finally, lymphatic channels in the head, neck and upper extremities drain to the jugular lymph sacs. Additionally, a right and left thoracic duct form and connect the cisterna chyli with the jugular lymph sacs and form anastomoses that eventually produce the typical adult form. The lymph sacs then produce groups of lymph nodes in the fetal period. Migrating mesenchyme enters the lymph sacs and produces lymphatic networks, connective tissue, and other layers of the lymph nodes. Function The lymphatic system's primary function is to balance the volume of interstitial fluid and convey it and excess protein molecules into the venous circulation. The lymphatic system is also important in immune surveillance, defending the body against foreign particles and microorganisms. It does so by conveying antigens and leukocytes to lymph nodes, where antigen-primed and targeted lymphocytes and other immune cells are conveyed into the lymphatic vessels and blood vessels. In addition, the system has a role in the absorption of fat-soluble vitamins and fatty substances in the gut via the gastrointestinal tract's lacteals within the villi and the transport of this material into the venous circulation. Newly recognized lymphatic vessels are visible in the meninges relating to cerebrospinal fluid (CSF) outflow from the central nervous system. Finally, lymphatics may play a role in the clearance of ocular fluid via the lymphatic-like Schlemm canals. Clinical Significance Leaks of lymphatic fluid occur when the lymphatic vessels are damaged. In the abdomen, lymphatic vessel damage may occur during surgery, especially during retroperitoneal procedures such as repairing an abdominal aortic aneurysm. These leaks tend to be mild, and the vessels in the peritoneum and mesentery eventually absorb the lymphatic fluid or chyle. However, when the thoracic duct is injured in the chest, the chyle leak can be extensive. In most cases, conservative care with a no-fat diet (medium chain triglycerides) or total parenteral nutrition is unsuccessful. In most cases, if the injury to the thoracic duct was surgical, a surgical procedure is required to tie off the duct. If the thoracic duct is injured in the cervical region, then inserting a drainage tube and adopting a low-fat diet will help seal the leak. However, thoracic duct injury in the chest cavity usually requires drainage and surgery. It is rare for the thoracic segment of the thoracic duct to seal on its own. In terms of accumulation of chyle in the thorax (i.e., chylothorax), if a patient has an injury to the thoracic duct in the thorax below the T5 vertebral level, then fluid will collect in only the right pleural cavity. If the injury is to the thoracic duct in the thorax above the T5 vertebral level, then fluid will appear in both pleural cavities. Other Issues The lymphatic system is prone to disorders like the venous and arterial circulatory systems. Developmental or functional defects of the lymphatic system cause lymphedema. When this occurs, the lymphatic system is unable to sufficiently drain lymphatic fluid resulting in its accumulation and swelling of the territory. Lymphedema, this swelling due to the accumulation of lymph, is classified as primary or secondary. Primary lymphedema is an inherited disorder where the lymphatic system development has been disrupted, causing absent or malformed lymphatic tissues. This condition often presents soon after birth, but some conditions may present later in life (e.g., at puberty or later adulthood). There are no effective treatments for primary lymphedema. Past surgical treatments were found to be mutilating and are no longer implemented. The present-day treatment revolves around compression stockings, pumps, and constrictive garments. Secondary lymphedema is an acquired disorder involving lymphatic system dysfunction that may result from many causes, including cancer, infection, trauma, or surgery. The treatment of secondary lymphedema depends on the cause. Oncological and other surgeries may result in secondary lymphedema due to the removal or biopsy of lymph nodes or lymphatic vessels. Non-surgical lymphedema may result from malignancies, obstruction within the lymphatic system, infection, or deep vein thrombosis. In most cases of obstructive secondary lymphedema, the drainage will resume if the inciting cause is removed, although some individuals may need to wear compressive stockings permanently. Also, physical therapy may help alleviate lymphedema when the extremities are involved. There is no absolute cure for lymphedema, but diagnosis and careful management can help to minimize complications. Lymphomas are cancers that arise from the cells of the lymphatic system. There are numerous types of lymphoma, but they are grouped into Hodgkin lymphoma and non-Hodgkin lymphoma. Lymphomas usually arise from the malignant transformation of specific lymphocytes in the lymphatic vessels or lymph nodes in the gastrointestinal tract, neck, axilla, or groin. Symptoms of lymphoma may include night sweats, fever, fatigue, itching, and weight loss. Cancers originating outside of the lymphatic system often spread via the lymphatic vessels and may involve regional lymph nodes serving the impacted organs or tissues. Lymphadenitis occurs when the lymph nodes become inflamed or enlarged. The cause is usually an adjacent bacterial infection but may also involve viruses or fungi. The lymph nodes usually enlarge and become tender. Lymphatic filariasis, or elephantiasis, is a very common mosquito-borne disorder caused by a parasite found in tropical and subtropical areas of the world, including Africa, Asia, the Pacific, the Caribbean, and South America. This condition involves parasitic microscopic nematodes (roundworms) that infect the lymphatic system and rapidly multiply and disrupt lymphatic function. Many infected individuals may have no outward symptoms, although the kidneys and lymphatic tissues may be damaged and dysfunctional. Symptomatic individuals may present with disfigurement caused by significant lymphedema and elephantiasis (thickening of the skin, particularly the extremities). The parasite may also cause hydrocele, an enlargement of the scrotum due to the accumulation of fluid, which may result from obstruction of the lymph nodes or vessels in the groin. Individuals presenting with symptoms have poorly draining lymphatics, often involving the extremities, resulting in huge extremities and marked disability. Lymphatic filariasis is the most common cause of disfigurement in the world, and it is the second most common cause of long-term disability. (credits: NIH)
In this episode of the NCS Podcast Hot Topics series, host Richard Choi, DO, FNCS, speaks with Katharina Busl, MD, MS, FNCS, division chief of neurocritical care at the University of Florida and assistant editor for Neurocritical Care journal. They explore new research on cerebrospinal fluid (CSF) clearance after aneurysmal subarachnoid hemorrhage. They also discuss the study Prospective Trial of Cerebrospinal Fluid Filtration After Aneurysmal Subarachnoid Hemorrhage: The Lumbar Catheter Extension (PILLAR XT) Trial, which evaluates a dual-lumen intrathecal catheter designed to filter CSF and accelerate removal of red blood cells and inflammatory byproducts. Their conversation highlights the rationale behind CSF drainage, how prior work like the Early Drain trial shaped the field, and what this early-phase device trial reveals about feasibility, safety, and reductions in CSF RBC and protein levels. Dr. Bussel and Dr. Choi also touch on implementation challenges and the need for larger trials before this approach can move into broader clinical use. The views expressed on the NCS Podcast are solely those of the hosts and guests and do not necessarily reflect the opinions or official positions of the Neurocritical Care Society.
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